<?xml version="1.0" encoding="UTF-8"?>
<!DOCTYPE article PUBLIC "-//NLM//DTD JATS (Z39.96) Journal Publishing DTD v1.3 20210610//EN" "JATS-journalpublishing1-3.dtd">
<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">nefr</journal-id><journal-title-group><journal-title xml:lang="ru">Нефрология</journal-title><trans-title-group xml:lang="en"><trans-title>Nephrology (Saint-Petersburg)</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1561-6274</issn><issn pub-type="epub">2541-9439</issn><publisher><publisher-name>Pavlov First Saint-Petersburg State Medical University</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.36485/1561-6274-2021-25-2-35-42</article-id><article-id custom-type="elpub" pub-id-type="custom">nefr-1941</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ОБЗОРЫ И ЛЕКЦИИ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>REVIEWS AND LECTURES</subject></subj-group></article-categories><title-group><article-title>Роль эпигенетических механизмов в патогенезе диабетической нефропатии</article-title><trans-title-group xml:lang="en"><trans-title>The role of epigenetic mechanisms in the pathogenesis of diabetic nephropathy</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-4973-039X</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Айтбаев</surname><given-names>К. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Aitbaev</surname><given-names>K. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Айтбаев Кубаныч Авенович, д-р мед. наук</p><p>720040, Кыргызстан, г. Бишкек, ул. Т. Молдо, д. 3</p><p>Тел.: (312) 66-25-13</p></bio><bio xml:lang="en"><p>Kubanych A. Aitbaev, MD, PhD, DMedSci; Head of the Department of Pathological Physiology; Member of the Board of the Society of Chronic Kidney Disease Specialists</p><p>720040, Kyrgyzstan, Bishkek, T. Moldo, Street, 3</p><p>Phone: (312) 66-25-13</p></bio><email xlink:type="simple">kaitbaev@yahoo.com</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-8513-9279</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Муркамилов</surname><given-names>И. Т.</given-names></name><name name-style="western" xml:lang="en"><surname>Murkamilov</surname><given-names>I. T.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Муркамилов Илхом Торобекович, канд. мед. наук, исполняющий обязанности доцента кафедры факультетской терапии; старший преподаватель кафедры терапии №2 медицинского факультета</p><p>720020, г. Бишкек, ул. Ахунбаева, д. 92</p><p>Тел.: (312) 62-09-91</p></bio><bio xml:lang="en"><p>Ilkhom T. Murkamilov, MD, PhD; acting associate professor of the Department of faculty therapy; Senior lecturer; Chairman of the board of Chronic Kidney Disease specialists</p><p>720020, Kyrgyzstan, Bishkek, Akhunbaev Street, 92</p><p>Phone: (312) 62-09-91</p></bio><email xlink:type="simple">murkamilov.i@mail.ru</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-2682-4417</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Фомин</surname><given-names>В. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Fomin</surname><given-names>V V</given-names></name></name-alternatives><bio xml:lang="ru"><p>Чл.-кор. РАН Виктор Викторович Фомин, д-р мед. наук, зав. каф. факультетской терапии №1, проректор по клинической работе и дополнительному профессиональному образованию</p><p>119146, Россия, Москва, ул. Большая Пироговская, д. 6</p><p>Тел.: 8 (499) 248-62-22</p></bio><bio xml:lang="en"><p>Сorresponding member of RAS Viktor V. Fomin, MD, PhD, DMedSci; Head of the Department of Faculty Therapy No.1</p><p>119146, Russia, Moscow, 6 Bolshaya Pirogovskaya, Street 6</p><p>Phone: +7 (499) 248-62-22</p></bio><email xlink:type="simple">fomin@mma.ru</email><xref ref-type="aff" rid="aff-3"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-7653-0433</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Муркамилова</surname><given-names>Ж. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Murkamilova</surname><given-names>Zh. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Муркамилова Жамила Абдилалимовна, заочный аспирант</p><p>Кыргызстан, 720000, г. Бишкек, ул. Киевская, д. 44</p><p>Тел.: (+996) 552435009</p></bio><bio xml:lang="en"><p>Correspondence graduate student Zhamila A. Murkamilova, MD; Department of Therapy No. 2</p><p>720000, Kyrgyzstan, Bishkek, Kiev, Street, 44</p><p>Phone: (+996) 552435009</p></bio><email xlink:type="simple">murkamilovazh.t@mail.ru</email><xref ref-type="aff" rid="aff-4"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-0632-6653</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Юсупов</surname><given-names>Ф. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Yusupov</surname><given-names>F. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Фуркат Абдулахатович Юсупов, д-р мед. наук, Зав. каф. неврологии, психиатрии и нейрохирургии медицинского факультета Ошского; Главный невролог Южного региона</p><p>714000, г. Ош, ул. Ленина, д. 331</p><p>Тел.: (+996) 557202071</p></bio><bio xml:lang="en"><p>Furkat A. Yusupov, MD, PhD; Head of the Department of neurology, psychiatry and medicinal genetics of medicinal</p><p>faculty; Board member of Chronic Kidney Disease specialists</p><p>714000, Kyrgyzstan, Osh, Lenin Street, 331</p><p>Phone: (+996) 557202071</p></bio><email xlink:type="simple">furcat_y@mail.ru</email><xref ref-type="aff" rid="aff-5"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>НИИ молекулярной биологии и медицины при Национальном центре кардиологии и терапии им. акад. Мирсаида Миррахимова</institution><country>Кыргызстан</country></aff><aff xml:lang="en"><institution>Research Institute of Molecular Biology and Medicine</institution><country>Kyrgyzstan</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>Кыргызская государственная медицинская академия им. И.К. Ахунбаева; Кыргызско-Российский славянский университет</institution><country>Кыргызстан</country></aff><aff xml:lang="en"><institution>I.K.Akhunbaev Kyrgyz State Medical Academy</institution><country>Kyrgyzstan</country></aff></aff-alternatives><aff-alternatives id="aff-3"><aff xml:lang="ru"><institution>Первый Московский государственный медицинский университет им. И.М. Сеченова</institution><country>Россия</country></aff><aff xml:lang="en"><institution>I.M. Sechenov First Moscow State Medical University</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-4"><aff xml:lang="ru"><institution>Кыргызско-Российский Славянский университет</institution><country>Кыргызстан</country></aff><aff xml:lang="en"><institution>Kyrgyz Russian Slavic University</institution><country>Kyrgyzstan</country></aff></aff-alternatives><aff-alternatives id="aff-5"><aff xml:lang="ru"><institution>Ошский государственный университет</institution><country>Кыргызстан</country></aff><aff xml:lang="en"><institution>Osh State University</institution><country>Kyrgyzstan</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2021</year></pub-date><pub-date pub-type="epub"><day>13</day><month>02</month><year>2021</year></pub-date><volume>25</volume><issue>2</issue><fpage>35</fpage><lpage>42</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Айтбаев К.А., Муркамилов И.Т., Фомин В.В., Муркамилова Ж.А., Юсупов Ф.А., 2021</copyright-statement><copyright-year>2021</copyright-year><copyright-holder xml:lang="ru">Айтбаев К.А., Муркамилов И.Т., Фомин В.В., Муркамилова Ж.А., Юсупов Ф.А.</copyright-holder><copyright-holder xml:lang="en">Aitbaev K.A., Murkamilov I.T., Fomin V.V., Murkamilova Z.A., Yusupov F.A.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://journal.nephrolog.ru/jour/article/view/1941">https://journal.nephrolog.ru/jour/article/view/1941</self-uri><abstract><p>Диабетическая нефропатия (ДН) является хроническим осложнением диабета и наиболее распространенной причиной развития терминальной стадии почечной недостаточности (ТСПН). Были предложены многочисленные факторы, как способствующие развитию ДН, так и участвующие в её патогенезе. Однако молекулярные механизмы, которые приводят к развитию ДН, остаются на сегодняшний день не вполне понятными. В последнее время с развитием высокопроизводительных технологий появляются доказательства, свидетельствующие об эпигенетических механизмах регуляции экспрессии генов, включая метилирование ДНК, некодирующие РНК и гистоновые модификации, которые играют ключевую роль в патогенезе ДН посредством вторичной регуляции генов. Все эти данные могут способствовать созданию новых, более эффективных диагностических и терапевтических технологий для ДН.</p></abstract><trans-abstract xml:lang="en"><p>Diabetic nephropathy (DN) is a chronic complication of diabetes and the most common cause of the end-stage renal disease (ESRD). Numerous factors have been considered, both contributing to the development of DN, and participating in its pathogenesis. However, to date, the molecular mechanisms, that lead to the development of DN, remain not fully understood. Recently, with the development of high-performance technologies, evidence demonstrating epigenetic mechanisms of regulation of gene expression, including DNA methylation, non-coding RNAs, and histone modifications that play a key role in the pathogenesis of DN through the secondary regulation of genes are starting to appear. All these data can contribute to the creation of new, more effective diagnostic and therapeutic technologies for DN.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>диабетическая нефропатия</kwd><kwd>эпигенетика</kwd><kwd>метилирование ДНК</kwd><kwd>некодирующие РНК</kwd><kwd>гистоновые модификации</kwd></kwd-group><kwd-group xml:lang="en"><kwd>diabetic nephropathy</kwd><kwd>epigenetics</kwd><kwd>DNA methylation</kwd><kwd>non-coding RNA</kwd><kwd>histone modification</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Шестакова МВ, Шамхалова МШ, Ярек-Мартынова ИЯ и др. Сахарный диабет и хроническая болезнь почек: достижения, нерешенные проблемы и перспективы лечения. Сахарный диабет 2011; 14 (1): 81-88</mixed-citation><mixed-citation xml:lang="en">Shestakova MV, Shamkhalova MS, Yarek-Martynova IY et al. Diabetes mellitus and chronic kidney disease: achievements, unresolved problems, and prospects for therapy. Diabetes mellitus 2011;14:1:81-88</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Камышова ЕС, Бобкова ИН, Кутырина ИМ. Современные представления о роли микроРНК при диабетической нефропатии: потенциальные биомаркеры и мишени таргетной терапии. Сахарный диабет 2017; 20 (1):42-50. https://doi.org/10.14341/DM8237</mixed-citation><mixed-citation xml:lang="en">Kamyshova ES, Bobkova IN, Kutyrina IM. New insights on microRNAs in diabetic nephropathy: potential biomarkers for diagnosis and therapeutic targets. Diabetes mellitus 2017;20:1:42-50. https://doi.org/10.14341/DM8237</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Regele F, Jelencsics K, Shiffman D et al. Genome-wide studies to identify risk factors for kidney disease with a focus on patients with diabetes. Nephrology Dialysis Transplantation 2015; 30 (4): iv26–iv34. https://doi.org/10.1093/ndt/gfv087</mixed-citation><mixed-citation xml:lang="en">Regele F, Jelencsics K, Shiffman D et al. Genome-wide studies to identify risk factors for kidney disease with a focus on patients with diabetes. Nephrology Dialysis Transplantation 2015; 30 (4): iv26–iv34. https://doi.org/10.1093/ndt/gfv087</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Cowie CC, Port FK, Wolfe RA et al. Disparities in incidence of diabetic endstage renal disease according to race and type of diabetes. New England Journal of Medicine 1989; 321(16):1074–1079. https://doi.org/10.1056/NEJM198910193211603</mixed-citation><mixed-citation xml:lang="en">Cowie CC, Port FK, Wolfe RA et al. Disparities in incidence of diabetic endstage renal disease according to race and type of diabetes. New England Journal of Medicine 1989; 321(16):1074–1079. https://doi.org/10.1056/NEJM198910193211603</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Pirola L, Balcerczyk A, Okabe J, El-Osta A. Epigenetic phenomena linked to diabetic complications. Nature Reviews Endocrinology 2010; 6(12):665–675. https://doi.org/10.1038/nrendo.2010.188</mixed-citation><mixed-citation xml:lang="en">Pirola L, Balcerczyk A, Okabe J, El-Osta A. Epigenetic phenomena linked to diabetic complications. Nature Reviews Endocrinology 2010; 6(12):665–675. https://doi.org/10.1038/nrendo.2010.188</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Portela A, Esteller M. Epigenetic modifications and human disease. Nature Biotechnology 2010; 28 (10):1057–1068. https:// doi.org/10.1038/nbt.1685</mixed-citation><mixed-citation xml:lang="en">Portela A, Esteller M. Epigenetic modifications and human disease. Nature Biotechnology 2010; 28 (10):1057–1068. https:// doi.org/10.1038/nbt.1685</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Thomas MC. Epigenetic mechanisms in diabetic kidney disease. Current Diabetes Reports 2016;16:3:31. https://doi.org/10.1007/s11892-016-0723-9</mixed-citation><mixed-citation xml:lang="en">Thomas MC. Epigenetic mechanisms in diabetic kidney disease. Current Diabetes Reports 2016;16:3:31. https://doi.org/10.1007/s11892-016-0723-9</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Jones PA. Functions of DNA methylation: islands, startsites, gene bodies and beyond. Nature Reviews Genetics 2012; 13 (7):484–492. https://doi.org/10.1038/nrg3230</mixed-citation><mixed-citation xml:lang="en">Jones PA. Functions of DNA methylation: islands, startsites, gene bodies and beyond. Nature Reviews Genetics 2012; 13 (7):484–492. https://doi.org/10.1038/nrg3230</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Barres R, Osler ME, Yan J et al. Non-CpG methylation of the PGC-1α promoter through DNMT3B controls mitochondrial density. Cell Metabolism 2009; 10(3):189–198. https://doi.org/10.1016/j.cmet.2009.07.011</mixed-citation><mixed-citation xml:lang="en">Barres R, Osler ME, Yan J et al. Non-CpG methylation of the PGC-1α promoter through DNMT3B controls mitochondrial density. Cell Metabolism 2009; 10(3):189–198. https://doi.org/10.1016/j.cmet.2009.07.011</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Marumo T, Yagi S, Kawarazaki W et al. Diabetes induces aberrant DNA methylation in the proximal tubules of the kidney. Journal of the American Society of Nephrology 2015; 26 (10):2388–2397. https://doi.org/10.1681/ASN.2014070665</mixed-citation><mixed-citation xml:lang="en">Marumo T, Yagi S, Kawarazaki W et al. Diabetes induces aberrant DNA methylation in the proximal tubules of the kidney. Journal of the American Society of Nephrology 2015; 26 (10):2388–2397. https://doi.org/10.1681/ASN.2014070665</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Wu R, Wang L, Yin R, et al. Epigenetics/epigenomics and prevention by curcumin of early stages of inflammatorydriven colon cancer. Molecular Carcinogenesis 2020. https://doi.org/10.1002/mc.23146</mixed-citation><mixed-citation xml:lang="en">Wu R, Wang L, Yin R, et al. Epigenetics/epigenomics and prevention by curcumin of early stages of inflammatorydriven colon cancer. Molecular Carcinogenesis 2020. https://doi.org/10.1002/mc.23146</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Gu HF. Genetic and epigenetic studies in diabetic kidney disease. Frontiers in genetics 2019;10:507. https://doi.org/10.3389/fgene.2019.00507</mixed-citation><mixed-citation xml:lang="en">Gu HF. Genetic and epigenetic studies in diabetic kidney disease. Frontiers in genetics 2019;10:507. https://doi.org/10.3389/fgene.2019.00507</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Bell CG, Teschendorff AE, Rakyan VK et al. Genome-wide DNA methylation analysis for diabetic nephropathy in type 1 diabetes mellitus. BMC Medical Genomics 2010;3:33. https://doi.org/10.1186/1755-8794-3-33</mixed-citation><mixed-citation xml:lang="en">Bell CG, Teschendorff AE, Rakyan VK et al. Genome-wide DNA methylation analysis for diabetic nephropathy in type 1 diabetes mellitus. BMC Medical Genomics 2010;3:33. https://doi.org/10.1186/1755-8794-3-33</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Sapienza C, Lee J, Powell J et al. DNA methylation profiling identifies epigenetic differences between diabetes patients with ESRD and diabetes patients without nephropathy. Epigenetics 2011; 6(1):20–28. https://doi.org/10.4161/epi.6.1.13362</mixed-citation><mixed-citation xml:lang="en">Sapienza C, Lee J, Powell J et al. DNA methylation profiling identifies epigenetic differences between diabetes patients with ESRD and diabetes patients without nephropathy. Epigenetics 2011; 6(1):20–28. https://doi.org/10.4161/epi.6.1.13362</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Hasegawa K, Wakino S, Simic P et al. Renal tubular sirt1 attenuates diabetic albuminuria by epigenetically suppressing claudin-1 overexpression in podocytes. Nature Medicine 2013; 19(11):1496–1504. https://doi.org/10.1038/nm.3363</mixed-citation><mixed-citation xml:lang="en">Hasegawa K, Wakino S, Simic P et al. Renal tubular sirt1 attenuates diabetic albuminuria by epigenetically suppressing claudin-1 overexpression in podocytes. Nature Medicine 2013; 19(11):1496–1504. https://doi.org/10.1038/nm.3363</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Ko Y-A, Mohtat D, Suzuki M et al. Cytosine methylation changes in enhancer regions of core pro-fibrotic genes characterize kidney fibrosis development. Genome Biology 2013;14(10): article R108. https://doi.org/10.1186/gb-2013-14-10-r108</mixed-citation><mixed-citation xml:lang="en">Ko Y-A, Mohtat D, Suzuki M et al. Cytosine methylation changes in enhancer regions of core pro-fibrotic genes characterize kidney fibrosis development. Genome Biology 2013;14(10): article R108. https://doi.org/10.1186/gb-2013-14-10-r108</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Bechtel W, McGoohan S, Zeisbergetal EM. Methylation determines fibroblast activation and fibrogenesis in the kidney. Nature Medicine 2010;5:16:544–550. https://doi.org/10.1038/nm.2135</mixed-citation><mixed-citation xml:lang="en">Bechtel W, McGoohan S, Zeisbergetal EM. Methylation determines fibroblast activation and fibrogenesis in the kidney. Nature Medicine 2010;5:16:544–550. https://doi.org/10.1038/nm.2135</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Pirola L, Balcerczyk A, Tothill RW et al. Genome-wide analysis distinguishes hyperglycemia regulated epigenetic signatures of primary vascular cells. Genome Research 2011; 21(10):1601–1615. https://doi.org/10.1101/gr.116095.110</mixed-citation><mixed-citation xml:lang="en">Pirola L, Balcerczyk A, Tothill RW et al. Genome-wide analysis distinguishes hyperglycemia regulated epigenetic signatures of primary vascular cells. Genome Research 2011; 21(10):1601–1615. https://doi.org/10.1101/gr.116095.110</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Liang F, Holt I, Pertea G et al. Gene index analysis of the human genome estimates approximately 120,000 genes. Nature Genetics 2000; 25(2): 239–240. https://doi.org/10.1038/76126</mixed-citation><mixed-citation xml:lang="en">Liang F, Holt I, Pertea G et al. Gene index analysis of the human genome estimates approximately 120,000 genes. Nature Genetics 2000; 25(2): 239–240. https://doi.org/10.1038/76126</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Kapranov P, Cawley SE, Drenkow J et al. Large-scale transcriptional activity in chromosomes 21 and 22. Science 2002; 296 (5569):916–919. Doi: 10.1126/science.1068597</mixed-citation><mixed-citation xml:lang="en">Kapranov P, Cawley SE, Drenkow J et al. Large-scale transcriptional activity in chromosomes 21 and 22. Science 2002; 296 (5569):916–919. Doi: 10.1126/science.1068597</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Djebali S, Davis CA, Merkel A et al. Landscape of transcription in human cells. Nature 2012;489:101–108. https://doi.org/10.1038/nature11233</mixed-citation><mixed-citation xml:lang="en">Djebali S, Davis CA, Merkel A et al. Landscape of transcription in human cells. Nature 2012;489:101–108. https://doi.org/10.1038/nature11233</mixed-citation></citation-alternatives></ref><ref id="cit22"><label>22</label><citation-alternatives><mixed-citation xml:lang="ru">Consortium Encode Project. An integrated encyclopedia of DNA elements in the human genome. Nature 2012; 489: 57–74. https://doi.org/10.1038/nature11247</mixed-citation><mixed-citation xml:lang="en">Consortium Encode Project. An integrated encyclopedia of DNA elements in the human genome. Nature 2012; 489: 57–74. https://doi.org/10.1038/nature11247</mixed-citation></citation-alternatives></ref><ref id="cit23"><label>23</label><citation-alternatives><mixed-citation xml:lang="ru">Okazaki Y, Furuno M, Kasukawa T et al. Analysis of the mouse transcriptome based on functional annotation of 60,770 full-length cDNAs. Nature 2002; 420: 563–573. https://doi.org/10.1038/nature01266</mixed-citation><mixed-citation xml:lang="en">Okazaki Y, Furuno M, Kasukawa T et al. Analysis of the mouse transcriptome based on functional annotation of 60,770 full-length cDNAs. Nature 2002; 420: 563–573. https://doi.org/10.1038/nature01266</mixed-citation></citation-alternatives></ref><ref id="cit24"><label>24</label><citation-alternatives><mixed-citation xml:lang="ru">Bartel DP. MicroRNAs: target recognition and regulatory functions. Cell 2009;136 (2):215–233. https://doi.org/10.1016/j.cell.2009.01.002</mixed-citation><mixed-citation xml:lang="en">Bartel DP. MicroRNAs: target recognition and regulatory functions. Cell 2009;136 (2):215–233. https://doi.org/10.1016/j.cell.2009.01.002</mixed-citation></citation-alternatives></ref><ref id="cit25"><label>25</label><citation-alternatives><mixed-citation xml:lang="ru">Kozomara A, Griffiths-Jones S. miRBase: annotating high confidence microRNAs using deep sequencing data. Nucleic Acids Research 2014;1:42:D68–D73. https://doi.org/10.1093/nar/gkt1181</mixed-citation><mixed-citation xml:lang="en">Kozomara A, Griffiths-Jones S. miRBase: annotating high confidence microRNAs using deep sequencing data. Nucleic Acids Research 2014;1:42:D68–D73. https://doi.org/10.1093/nar/gkt1181</mixed-citation></citation-alternatives></ref><ref id="cit26"><label>26</label><citation-alternatives><mixed-citation xml:lang="ru">Sun Y, Koo S, White N et al. Development of a micro-array to detect human and mouse microRNAs and characterization of expression in human organs. Nucleic acids research 2004; 32(22): article e188. https://doi.org/10.1093/nar/gnh186</mixed-citation><mixed-citation xml:lang="en">Sun Y, Koo S, White N et al. Development of a micro-array to detect human and mouse microRNAs and characterization of expression in human organs. Nucleic acids research 2004; 32(22): article e188. https://doi.org/10.1093/nar/gnh186</mixed-citation></citation-alternatives></ref><ref id="cit27"><label>27</label><citation-alternatives><mixed-citation xml:lang="ru">Tian Z, Greene AS, Pietrusz JL et al. MicroRNA-target pairs in the rat kidney identified by microRNA microarray, proteomic, and bioinformatic analysis. Genome Research 2008; 18(3):404–411. https://doi.org/10.1101/gr.6587008</mixed-citation><mixed-citation xml:lang="en">Tian Z, Greene AS, Pietrusz JL et al. MicroRNA-target pairs in the rat kidney identified by microRNA microarray, proteomic, and bioinformatic analysis. Genome Research 2008; 18(3):404–411. https://doi.org/10.1101/gr.6587008</mixed-citation></citation-alternatives></ref><ref id="cit28"><label>28</label><citation-alternatives><mixed-citation xml:lang="ru">Wu H, Kong L, Zhou S et al. The role of microRNAs in diabetic nephropathy. Journal of Diabetes Research 2014; 2014: article ID 920134, 12 pages. https://doi.org/10.1155/2014/920134</mixed-citation><mixed-citation xml:lang="en">Wu H, Kong L, Zhou S et al. The role of microRNAs in diabetic nephropathy. Journal of Diabetes Research 2014; 2014: article ID 920134, 12 pages. https://doi.org/10.1155/2014/920134</mixed-citation></citation-alternatives></ref><ref id="cit29"><label>29</label><citation-alternatives><mixed-citation xml:lang="ru">Kato M, Zhang J, Wang M et al. MicroRNA-192 in diabetic kidney glomeruli and its function in TGF-β-induced collagen expression via inhibition of E-box repressors. Proceedings of the National Academy of Sciences of the United States of America 2007;104(9):3432–3437. https://doi.org/10.1073/pnas.0611192104</mixed-citation><mixed-citation xml:lang="en">Kato M, Zhang J, Wang M et al. MicroRNA-192 in diabetic kidney glomeruli and its function in TGF-β-induced collagen expression via inhibition of E-box repressors. Proceedings of the National Academy of Sciences of the United States of America 2007;104(9):3432–3437. https://doi.org/10.1073/pnas.0611192104</mixed-citation></citation-alternatives></ref><ref id="cit30"><label>30</label><citation-alternatives><mixed-citation xml:lang="ru">Chung ACK, Huang XR, Meng X, Lan XY. miR-192 mediates TGF-β/Smad3-driven renal fibrosis. Journal of the American Society of Nephrology 2010; 21(8):1317–1325. https://doi.org/10.1681/ASN.2010020134</mixed-citation><mixed-citation xml:lang="en">Chung ACK, Huang XR, Meng X, Lan XY. miR-192 mediates TGF-β/Smad3-driven renal fibrosis. Journal of the American Society of Nephrology 2010; 21(8):1317–1325. https://doi.org/10.1681/ASN.2010020134</mixed-citation></citation-alternatives></ref><ref id="cit31"><label>31</label><citation-alternatives><mixed-citation xml:lang="ru">Krupa A, Jenkins R, DongLuo D et al. Loss of microRNA-192 promotes fibrogenesis in diabetic nephropathy. Journal of the American Society of Nephrology 2010; 21(3):438–447. https://doi.org/10.1681/ASN.2009050530</mixed-citation><mixed-citation xml:lang="en">Krupa A, Jenkins R, DongLuo D et al. Loss of microRNA-192 promotes fibrogenesis in diabetic nephropathy. Journal of the American Society of Nephrology 2010; 21(3):438–447. https://doi.org/10.1681/ASN.2009050530</mixed-citation></citation-alternatives></ref><ref id="cit32"><label>32</label><citation-alternatives><mixed-citation xml:lang="ru">Wang B, Herman-Edelstein M, Koh P et al. E-cadherin expression is regulated by miR-192/215 by a mechanism that is independent of the profibrotic effects of transforming growth factor-β. Diabetes 2010;59(7):1794–1802. https://doi.org/10.2337/db09-1736</mixed-citation><mixed-citation xml:lang="en">Wang B, Herman-Edelstein M, Koh P et al. E-cadherin expression is regulated by miR-192/215 by a mechanism that is independent of the profibrotic effects of transforming growth factor-β. Diabetes 2010;59(7):1794–1802. https://doi.org/10.2337/db09-1736</mixed-citation></citation-alternatives></ref><ref id="cit33"><label>33</label><citation-alternatives><mixed-citation xml:lang="ru">Kato M, Natarajan R. Diabetic nephropathy-emerging epigenetic mechanisms. Nature Reviews Nephrology 2014;10 (9):517–530. https://doi.org/10.1038/nrneph.2014.116</mixed-citation><mixed-citation xml:lang="en">Kato M, Natarajan R. Diabetic nephropathy-emerging epigenetic mechanisms. Nature Reviews Nephrology 2014;10 (9):517–530. https://doi.org/10.1038/nrneph.2014.116</mixed-citation></citation-alternatives></ref><ref id="cit34"><label>34</label><citation-alternatives><mixed-citation xml:lang="ru">Deshpande SD, Putta S, Wang M et al. Transforming growth factor-β-induced cross talk between p53 and a MicroRNA in the pathogenesis of diabetic nephropathy. Diabetes 2013; 62(9):3151–3162. https://doi.org/10.2337/db13-0305</mixed-citation><mixed-citation xml:lang="en">Deshpande SD, Putta S, Wang M et al. Transforming growth factor-β-induced cross talk between p53 and a MicroRNA in the pathogenesis of diabetic nephropathy. Diabetes 2013; 62(9):3151–3162. https://doi.org/10.2337/db13-0305</mixed-citation></citation-alternatives></ref><ref id="cit35"><label>35</label><citation-alternatives><mixed-citation xml:lang="ru">Kato M, Natarajan R. MicroRNAs in diabetic nephropathy: Functions, biomarkers, and therapeutic targets. Annals of the New York Academy of Sciences 2015; 1353:72–88. https://doi.org/10.1111/nyas.12758</mixed-citation><mixed-citation xml:lang="en">Kato M, Natarajan R. MicroRNAs in diabetic nephropathy: Functions, biomarkers, and therapeutic targets. Annals of the New York Academy of Sciences 2015; 1353:72–88. https://doi.org/10.1111/nyas.12758</mixed-citation></citation-alternatives></ref><ref id="cit36"><label>36</label><citation-alternatives><mixed-citation xml:lang="ru">Putta S, Lanting L, Sun G, Lawson G, Kato M, Natarajan R. Inhibiting microRNA-192 ameliorates renal fibrosis in diabetic nephropathy. Journal of the American Society of Nephrology 2012; 23(3):458–469. https://doi.org/10.1681/ASN.2011050485</mixed-citation><mixed-citation xml:lang="en">Putta S, Lanting L, Sun G, Lawson G, Kato M, Natarajan R. Inhibiting microRNA-192 ameliorates renal fibrosis in diabetic nephropathy. Journal of the American Society of Nephrology 2012; 23(3):458–469. https://doi.org/10.1681/ASN.2011050485</mixed-citation></citation-alternatives></ref><ref id="cit37"><label>37</label><citation-alternatives><mixed-citation xml:lang="ru">Jia Y, Guan M, Zheng Z et al. MiRNAs in urine extracellular vesicles as predictors of early-stage diabetic nephropathy. Journal of Diabetes Research 2016; 2016: Article ID 7932765, 10 pages. https://doi.org/10.1155/2016/7932765</mixed-citation><mixed-citation xml:lang="en">Jia Y, Guan M, Zheng Z et al. MiRNAs in urine extracellular vesicles as predictors of early-stage diabetic nephropathy. Journal of Diabetes Research 2016; 2016: Article ID 7932765, 10 pages. https://doi.org/10.1155/2016/7932765</mixed-citation></citation-alternatives></ref><ref id="cit38"><label>38</label><citation-alternatives><mixed-citation xml:lang="ru">Kato M, Arce L, Wang M et al. A microRNA circuit mediates transforming growth factor-β1 autoregulation in renal glomerular mesangial cells. Kidney International 2011; 80(4): 358–368. https://doi.org/10.1038/ki.2011.43</mixed-citation><mixed-citation xml:lang="en">Kato M, Arce L, Wang M et al. A microRNA circuit mediates transforming growth factor-β1 autoregulation in renal glomerular mesangial cells. Kidney International 2011; 80(4): 358–368. https://doi.org/10.1038/ki.2011.43</mixed-citation></citation-alternatives></ref><ref id="cit39"><label>39</label><citation-alternatives><mixed-citation xml:lang="ru">Zhong X, Chung ACK, Chen HY et al. MiR-21 is a key therapeutic target for renal injury in a mouse model of type 2 diabetes. Diabetologia 2013; 56(3):663–674. https://doi.org/10.1007/s00125-012-2804-x</mixed-citation><mixed-citation xml:lang="en">Zhong X, Chung ACK, Chen HY et al. MiR-21 is a key therapeutic target for renal injury in a mouse model of type 2 diabetes. Diabetologia 2013; 56(3):663–674. https://doi.org/10.1007/s00125-012-2804-x</mixed-citation></citation-alternatives></ref><ref id="cit40"><label>40</label><citation-alternatives><mixed-citation xml:lang="ru">Rinn JL, Chang HY. Genome regulation by long noncoding RNAs. Annual Review of Biochemistry 2012; 81: 145–166. https://doi.org/10.1146/annurev-biochem-051410-092902</mixed-citation><mixed-citation xml:lang="en">Rinn JL, Chang HY. Genome regulation by long noncoding RNAs. Annual Review of Biochemistry 2012; 81: 145–166. https://doi.org/10.1146/annurev-biochem-051410-092902</mixed-citation></citation-alternatives></ref><ref id="cit41"><label>41</label><citation-alternatives><mixed-citation xml:lang="ru">Ponting CP, Oliver PL, Reik W. Evolution and functions of long noncoding RNAs. Cell 2009; 136 (4):629–641. https://doi.org/10.1016/j.cell.2009.02.006</mixed-citation><mixed-citation xml:lang="en">Ponting CP, Oliver PL, Reik W. Evolution and functions of long noncoding RNAs. Cell 2009; 136 (4):629–641. https://doi.org/10.1016/j.cell.2009.02.006</mixed-citation></citation-alternatives></ref><ref id="cit42"><label>42</label><citation-alternatives><mixed-citation xml:lang="ru">Ebert MS, Sharp PA. Emerging roles for natural microRNA sponges. Current Biology 2010; 20 (19):R858–R861. https://doi.org/10.1016/j.cub.2010.08.052</mixed-citation><mixed-citation xml:lang="en">Ebert MS, Sharp PA. Emerging roles for natural microRNA sponges. Current Biology 2010; 20 (19):R858–R861. https://doi.org/10.1016/j.cub.2010.08.052</mixed-citation></citation-alternatives></ref><ref id="cit43"><label>43</label><citation-alternatives><mixed-citation xml:lang="ru">Yang X, Tao L, Zhu J, Zhang S. Long Noncoding RNA FTX Reduces Hypertrophy of Neonatal Mouse Cardiac Myocytes and Regulates the PTEN/PI3K/Akt Signaling Pathway by Sponging MicroRNA-22. Medical Science Monitor: International Medical Journal of Experimental and Clinical Research 2019;25:9609-9617. https://doi.org/10.12659/MSM.919654</mixed-citation><mixed-citation xml:lang="en">Yang X, Tao L, Zhu J, Zhang S. Long Noncoding RNA FTX Reduces Hypertrophy of Neonatal Mouse Cardiac Myocytes and Regulates the PTEN/PI3K/Akt Signaling Pathway by Sponging MicroRNA-22. Medical Science Monitor: International Medical Journal of Experimental and Clinical Research 2019;25:9609-9617. https://doi.org/10.12659/MSM.919654</mixed-citation></citation-alternatives></ref><ref id="cit44"><label>44</label><citation-alternatives><mixed-citation xml:lang="ru">Reichelt-Wurm S, Wirtz T, Chittka D, et al. Glomerular expression pattern of long non-coding RNAs in the type 2 diabetes mellitus BTBR mouse model. Scientific reports 2019;9:1:1-13. https://doi.org/10.1038/s41598-019-46180-1 45. Kato M, Putta S, Wang M et al. TGF-β activates Akt kinase through a microRNA-dependent amplifying circuit targeting PTEN. Nature Cell Biology 2009;11(7):881–889. https://doi.org/10.1038/ncb1897</mixed-citation><mixed-citation xml:lang="en">Reichelt-Wurm S, Wirtz T, Chittka D, et al. Glomerular expression pattern of long non-coding RNAs in the type 2 diabetes mellitus BTBR mouse model. Scientific reports 2019;9:1:1-13. https://doi.org/10.1038/s41598-019-46180-1 45. Kato M, Putta S, Wang M et al. TGF-β activates Akt kinase through a microRNA-dependent amplifying circuit targeting PTEN. Nature Cell Biology 2009;11(7):881–889. https://doi.org/10.1038/ncb1897</mixed-citation></citation-alternatives></ref><ref id="cit45"><label>45</label><citation-alternatives><mixed-citation xml:lang="ru">Kato M, Dang V, Wang M et al. TGF-β induces acetylation of chromatin and of Ets-1 to alleviate repression of miR-192 in diabetic nephropathy. Science Signaling 2013;6 (278): article no. ra43. https://doi.org/10.1126/scisignal.2003389</mixed-citation><mixed-citation xml:lang="en">Kato M, Dang V, Wang M et al. TGF-β induces acetylation of chromatin and of Ets-1 to alleviate repression of miR-192 in diabetic nephropathy. Science Signaling 2013;6 (278): article no. ra43. https://doi.org/10.1126/scisignal.2003389</mixed-citation></citation-alternatives></ref><ref id="cit46"><label>46</label><citation-alternatives><mixed-citation xml:lang="ru">Kato M, Wang M, Chen Z et al. An endoplasmic reticulum stress-regulated lncRNA hosting a microRNA megacluster induces early features of diabetic nephropathy. Nature Communications 2016;7: article 12864. https://doi.org/10.1038/ncomms12864</mixed-citation><mixed-citation xml:lang="en">Kato M, Wang M, Chen Z et al. An endoplasmic reticulum stress-regulated lncRNA hosting a microRNA megacluster induces early features of diabetic nephropathy. Nature Communications 2016;7: article 12864. https://doi.org/10.1038/ncomms12864</mixed-citation></citation-alternatives></ref><ref id="cit47"><label>47</label><citation-alternatives><mixed-citation xml:lang="ru">Zhou Q, Chung ACK, Huang XR, Dong Y, Yu X, Lan HY. Identification of novel long noncoding rnas associated with TGF-β/ Smad3-mediated renal inflammation and fibrosis by RNA sequencing. American Journal of Pathology 2014;184(2):409-417. https:// doi.org/10.1016/j.ajpath.2013.10.007</mixed-citation><mixed-citation xml:lang="en">Zhou Q, Chung ACK, Huang XR, Dong Y, Yu X, Lan HY. Identification of novel long noncoding rnas associated with TGF-β/ Smad3-mediated renal inflammation and fibrosis by RNA sequencing. American Journal of Pathology 2014;184(2):409-417. https:// doi.org/10.1016/j.ajpath.2013.10.007</mixed-citation></citation-alternatives></ref><ref id="cit48"><label>48</label><citation-alternatives><mixed-citation xml:lang="ru">Long J, Badal SS, Ye Z et al. Long noncoding RNA Tug1 regulates mitochondrial bioenergetics in diabetic nephropathy. Journal of Clinical Investigation 2016;126(11):4205–4218. https:// doi.org/10.1172/JCI87927</mixed-citation><mixed-citation xml:lang="en">Long J, Badal SS, Ye Z et al. Long noncoding RNA Tug1 regulates mitochondrial bioenergetics in diabetic nephropathy. Journal of Clinical Investigation 2016;126(11):4205–4218. https:// doi.org/10.1172/JCI87927</mixed-citation></citation-alternatives></ref><ref id="cit49"><label>49</label><citation-alternatives><mixed-citation xml:lang="ru">Ji P, Diederichs S, Wang W et al. MALAT-1, a novel noncoding RNA, and thymosin β4 predict metastasis and survival in early-stage non-small cell lung cancer. Oncogene 2003;22 (39):8031–8041. https://doi.org/10.1038/sj.onc.1206928</mixed-citation><mixed-citation xml:lang="en">Ji P, Diederichs S, Wang W et al. MALAT-1, a novel noncoding RNA, and thymosin β4 predict metastasis and survival in early-stage non-small cell lung cancer. Oncogene 2003;22 (39):8031–8041. https://doi.org/10.1038/sj.onc.1206928</mixed-citation></citation-alternatives></ref><ref id="cit50"><label>50</label><citation-alternatives><mixed-citation xml:lang="ru">Liu J.-Y, Yao J, Li X.-M et al. Pathogenic role of lncRNA MALAT1 in endothelial cell dysfunction in diabetes mellitus. Cell Death and Disease 2014; 5: article ID e1506. https://doi.org/10.1038/cddis.2014.466</mixed-citation><mixed-citation xml:lang="en">Liu J.-Y, Yao J, Li X.-M et al. Pathogenic role of lncRNA MALAT1 in endothelial cell dysfunction in diabetes mellitus. Cell Death and Disease 2014; 5: article ID e1506. https://doi.org/10.1038/cddis.2014.466</mixed-citation></citation-alternatives></ref><ref id="cit51"><label>51</label><citation-alternatives><mixed-citation xml:lang="ru">Puthanveetil P, Chen S, Feng B, Gautam A, Chakrabarti S. Long non-coding RNA MALAT1 regulates hyperglycaemia induced inflammatory process in the endothelial cells. Journal of Cellular and Molecular Medicine 2015; 19 (6):1418–1425. https://doi.org/10.1111/jcmm.12576</mixed-citation><mixed-citation xml:lang="en">Puthanveetil P, Chen S, Feng B, Gautam A, Chakrabarti S. Long non-coding RNA MALAT1 regulates hyperglycaemia induced inflammatory process in the endothelial cells. Journal of Cellular and Molecular Medicine 2015; 19 (6):1418–1425. https://doi.org/10.1111/jcmm.12576</mixed-citation></citation-alternatives></ref><ref id="cit52"><label>52</label><citation-alternatives><mixed-citation xml:lang="ru">Kouzarides T. Chromatin modifications and their function. Cell 2007;128(4):693–705. https://doi.org/10.1016/j.cell.2007.02.005</mixed-citation><mixed-citation xml:lang="en">Kouzarides T. Chromatin modifications and their function. Cell 2007;128(4):693–705. https://doi.org/10.1016/j.cell.2007.02.005</mixed-citation></citation-alternatives></ref><ref id="cit53"><label>53</label><citation-alternatives><mixed-citation xml:lang="ru">Liu R, Lee K, He JC. Genetics and epigenetics of diabetic nephropathy. Kidney Diseases 2015; 1(1):42–51. https:// doi.org/10.1159/000381796</mixed-citation><mixed-citation xml:lang="en">Liu R, Lee K, He JC. Genetics and epigenetics of diabetic nephropathy. Kidney Diseases 2015; 1(1):42–51. https:// doi.org/10.1159/000381796</mixed-citation></citation-alternatives></ref><ref id="cit54"><label>54</label><citation-alternatives><mixed-citation xml:lang="ru">El-Osta A, Brasacchio D, Yao D et al. Transient high glucose causes persistent epigenetic changes and altered gene expression during subsequent normoglycemia. The Journal of Experimental Medicine 2008; 205:2409–2417. https://doi.org/10.1084/jem.20081188 56. Sun G, Reddy MA,Yuan H, Lanting L, Kato M, Natarajan R. Epigenetic histone methylation modulates fibrotic gene expression. Journal of the American Society of Nephrology 2010; 21 (12):2069–2080. https://doi.org/10.1681/ASN.2010060633</mixed-citation><mixed-citation xml:lang="en">El-Osta A, Brasacchio D, Yao D et al. Transient high glucose causes persistent epigenetic changes and altered gene expression during subsequent normoglycemia. The Journal of Experimental Medicine 2008; 205:2409–2417. https://doi.org/10.1084/jem.20081188 56. Sun G, Reddy MA,Yuan H, Lanting L, Kato M, Natarajan R. Epigenetic histone methylation modulates fibrotic gene expression. Journal of the American Society of Nephrology 2010; 21 (12):2069–2080. https://doi.org/10.1681/ASN.2010060633</mixed-citation></citation-alternatives></ref><ref id="cit55"><label>55</label><citation-alternatives><mixed-citation xml:lang="ru">Bock F, Shahzad K, Wang H et al. Activated protein C ameliorates diabetic nephropathy by epigenetically inhibiting the redox enzyme p66Shc. Proceedings of the National Academy of Sciences of the United States of America 2013; 110 (2): 648–653. https://doi.org/10.1073/pnas.1218667110</mixed-citation><mixed-citation xml:lang="en">Bock F, Shahzad K, Wang H et al. Activated protein C ameliorates diabetic nephropathy by epigenetically inhibiting the redox enzyme p66Shc. Proceedings of the National Academy of Sciences of the United States of America 2013; 110 (2): 648–653. https://doi.org/10.1073/pnas.1218667110</mixed-citation></citation-alternatives></ref><ref id="cit56"><label>56</label><citation-alternatives><mixed-citation xml:lang="ru">Sulaiman MK. Diabetic nephropathy: recent advances in pathophysiology and challenges in dietary management. Diabetology &amp; metabolic syndrome 2019;11:1:7. https://doi.org/10.1186/s13098-019-0403-4</mixed-citation><mixed-citation xml:lang="en">Sulaiman MK. Diabetic nephropathy: recent advances in pathophysiology and challenges in dietary management. Diabetology &amp; metabolic syndrome 2019;11:1:7. https://doi.org/10.1186/s13098-019-0403-4</mixed-citation></citation-alternatives></ref><ref id="cit57"><label>57</label><citation-alternatives><mixed-citation xml:lang="ru">Raval N, Kumawat A, Kalyane D, Kalia K, Tekade RK. Understanding molecular upsets in diabetic nephropathy to identify novel targets and treatment opportunities. Drug Discovery Today 2020. https://doi.org/10.1016/j.drudis.2020.01.008</mixed-citation><mixed-citation xml:lang="en">Raval N, Kumawat A, Kalyane D, Kalia K, Tekade RK. Understanding molecular upsets in diabetic nephropathy to identify novel targets and treatment opportunities. Drug Discovery Today 2020. https://doi.org/10.1016/j.drudis.2020.01.008</mixed-citation></citation-alternatives></ref><ref id="cit58"><label>58</label><citation-alternatives><mixed-citation xml:lang="ru">Li M, Guo Q, Cai H et al. miR-218 regulates diabetic nephropathy via targeting IKK-β and modulating NK-κB-mediated inflammation. Journal of cellular physiology 2020;235:4:3362-3371. https://doi.org/10.1002/jcp.29224</mixed-citation><mixed-citation xml:lang="en">Li M, Guo Q, Cai H et al. miR-218 regulates diabetic nephropathy via targeting IKK-β and modulating NK-κB-mediated inflammation. Journal of cellular physiology 2020;235:4:3362-3371. https://doi.org/10.1002/jcp.29224</mixed-citation></citation-alternatives></ref><ref id="cit59"><label>59</label><citation-alternatives><mixed-citation xml:lang="ru">Nascimento LR, Domingueti CP. MicroRNAs: new biomarkers and promising therapeutic targets for diabetic kidney disease. Brazilian Journal of Nephrology 2019. AHEAD. http:// dx.doi.org/10.1590/2175-8239-jbn-2018-0165</mixed-citation><mixed-citation xml:lang="en">Nascimento LR, Domingueti CP. MicroRNAs: new biomarkers and promising therapeutic targets for diabetic kidney disease. Brazilian Journal of Nephrology 2019. AHEAD. http:// dx.doi.org/10.1590/2175-8239-jbn-2018-0165</mixed-citation></citation-alternatives></ref><ref id="cit60"><label>60</label><citation-alternatives><mixed-citation xml:lang="ru">Lai JY, Luo J, O’Connor C et al. MicroRNA-21 in glomerular injury. Journal of the American Society of Nephrology 2015;26 (4):805–816. DOI: https://doi.org/10.1681/ASN.2013121274</mixed-citation><mixed-citation xml:lang="en">Lai JY, Luo J, O’Connor C et al. MicroRNA-21 in glomerular injury. Journal of the American Society of Nephrology 2015;26 (4):805–816. DOI: https://doi.org/10.1681/ASN.2013121274</mixed-citation></citation-alternatives></ref><ref id="cit61"><label>61</label><citation-alternatives><mixed-citation xml:lang="ru">Mohan A, Singh RS, Kumari M et al. Urinary exosomal microRNA-451-5p is a potential early biomarker of diabetic nephropathy in rats. PLoS ONE 2016;11(4):article ID e0154055. https:// doi.org/10.1371/journal.pone.0154055</mixed-citation><mixed-citation xml:lang="en">Mohan A, Singh RS, Kumari M et al. Urinary exosomal microRNA-451-5p is a potential early biomarker of diabetic nephropathy in rats. PLoS ONE 2016;11(4):article ID e0154055. https:// doi.org/10.1371/journal.pone.0154055</mixed-citation></citation-alternatives></ref><ref id="cit62"><label>62</label><citation-alternatives><mixed-citation xml:lang="ru">Dounousi E, Duni A, Leivaditis K et al. Improvements in the management of diabetic nephropathy. Review of Diabetic Studies 2015;12(1-2):119–133. https://doi.org/10.1900/RDS.2015.12.119</mixed-citation><mixed-citation xml:lang="en">Dounousi E, Duni A, Leivaditis K et al. Improvements in the management of diabetic nephropathy. Review of Diabetic Studies 2015;12(1-2):119–133. https://doi.org/10.1900/RDS.2015.12.119</mixed-citation></citation-alternatives></ref><ref id="cit63"><label>63</label><citation-alternatives><mixed-citation xml:lang="ru">Tonna S, El-Osta A, Cooper ME, Tikellis C. Metabolic memory and diabetic nephropathy: potential role for epigenetic mechanisms. Nature Reviews Nephrology 2010;6(6):332–341. https://doi.org/10.1038/nrneph.2010.55</mixed-citation><mixed-citation xml:lang="en">Tonna S, El-Osta A, Cooper ME, Tikellis C. Metabolic memory and diabetic nephropathy: potential role for epigenetic mechanisms. Nature Reviews Nephrology 2010;6(6):332–341. https://doi.org/10.1038/nrneph.2010.55</mixed-citation></citation-alternatives></ref></ref-list><fn-group><fn fn-type="conflict"><p>The authors declare that there are no conflicts of interest present.</p></fn></fn-group></back></article>
