[1]陈炜,许贞蓉.表观遗传学与代谢性心血管疾病的研究进展[J].心血管病学进展,2019,(6):902-906.[doi:10.16806/j.cnki.issn.1004-3934.2019.06.016]
 CHEN Wei,XU Zhenrong.Epigenetics and Cardiometabolic Disease[J].Advances in Cardiovascular Diseases,2019,(6):902-906.[doi:10.16806/j.cnki.issn.1004-3934.2019.06.016]
点击复制

表观遗传学与代谢性心血管疾病的研究进展()
分享到:

《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2019年6期
页码:
902-906
栏目:
综述
出版日期:
2019-09-25

文章信息/Info

Title:
Epigenetics and Cardiometabolic Disease
作者:
陈炜许贞蓉
(上海交通大学医学院附属新华医院老年医学科,上海 200092)
Author(s):
CHEN Wei XU Zhenrong
(Department of Geriatrics, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China)
关键词:
表观遗传学代谢性心血管疾病DNA甲基化组蛋白乙酰化胰岛素抵抗
Keywords:
Epigenetics Cardiometabolic disease DNA methylation Histone acetylation Insulin resistance
DOI:
10.16806/j.cnki.issn.1004-3934.2019.06.016
摘要:
DNA/组蛋白复合物的表观遗传学变化可通过快速改变染色质对转录因子的可及性来决定基因的活性。染色质修饰(DNA甲基化、组蛋白乙酰化等)在脂肪生成、胰岛素抵抗、巨噬细胞极化、免疫代谢、内皮功能障碍和代谢性心肌病(这些统归为代谢性心血管疾病的病理生理过程)中作为基因转录微调因子发挥重要作用。细胞特异性表观遗传信息的改变可以增进对心血管代谢过程的了解,为寻找代谢性心血管疾病新的治疗靶点从而研制个性化的治疗方案奠定基础。本综述将重点介绍表观遗传学如DNA甲基化、组蛋白乙酰化等在代谢性心血管疾病中的作用以及基于表观遗传学干预靶点的药物治疗进展。
Abstract:
Epigenetic changes in DNA/histone complexes can determine gene activity by rapidly altering the accessibility of chromatin to transcription factors. Chromatin modification (DNA methylation, histone acetylation, etc.) play an important role as gene transcriptional fine-tuning factors in the pathophysiological processes of cardiometabolic disease, including lipogenesis, insulin resistance, macrophage polarization, immune metabolism, endothelial dysfunction and metabolic cardiomyopathy. Specific changes in epigenetic information can enhance our understanding of cardiovascular metabolic processes and lay the foundation for finding new therapeutic targets for cardiometabolic disease and developing personalized treatment. This review focus on the role of epigenetics such as DNA methylation, histone acetylation in cardiometabolic disease, and advances in medication based on epigenetic interventions

参考文献/References:


[1] Brunet A, Berger SL. Epigenetics of aging and aging-related disease[J]. J Gerontol A Biol Sci Med Sci, 2014, 69(Suppl 1): S17-20.

[2] Handy DE, Castro R, Loscalzo J. Epigenetic modifications: basic mechanisms and role in cardiovascular disease[J]. Circulation, 2011, 123(19): 2145-2156.

[3] Tan Q, Christiansen L, Thomassen M, et al. Twins for epigenetic studies of human aging and development[J]. Ageing Res Rev, 2013, 12(1): 182-187.

[4] Fraga MF, Ballestar E, Paz MF, et al. Epigenetic differences arise during the lifetime of monozygotic twins[J]. Proc Natl Acad Sci U S A, 2005, 102(30): 10604-10609.

[5] Maegawa S, Lu Y, Tahara T, et al. Caloric restriction delays age-related methylation drift[J]. Nat Commun, 2017, 8(1): 539.

[6] Kohli RM, Zhang Y. TET enzymes, TDG and the dynamics of DNA demethylation[J]. Nature, 2013, 502(7472): 472-479.

[7] Miranda TB, Jones PA. DNA methylation: the nuts and bolts of repression[J]. J Cell Physiol, 2007, 213(2): 384-390.

[8] Shahbazian MD, Grunstein M. Functions of site-specific histone acetylation and deacetylation[J]. Annu Rev Biochem, 2007, 76: 75-100.

[9] Paneni F, Costantino S, Cosentino F. Molecular pathways of arterial aging[J]. Clin Sci (Lond), 2015, 128(2): 69-79.

[10] Cooper ME, El-Osta A. Epigenetics: mechanisms and implications for diabetic complications[J]. Circ Res, 2010, 107(12): 1403-1413.

[11] Gurha P, Marian AJ. Noncoding RNAs in cardiovascular biology and disease[J]. Circ Res, 2013, 113(12): e115-120.

[12] Mathiyalagan P, Keating ST, Du XJ, et al. Interplay of chromatin modifications and non-coding RNAs in the heart[J]. Epigenetics, 2014, 9(1): 101-112.

[13] Magistri M, Faghihi MA, St Laurent G, 3rd, et al. Regulation of chromatin structure by long noncoding RNAs: focus on natural antisense transcripts[J]. Trends Genet, 2012, 28(8): 389-396.

[14] Baccarelli A, Ghosh S. Environmental exposures, epigenetics and cardiovascular disease[J]. Curr Opin Clin Nutr Metab Care, 2012, 15(4): 323-329.

[15] Gut P, Verdin E. The nexus of chromatin regulation and intermediary metabolism[J]. Nature, 2013, 502(7472): 489-498.

[16] Tabak AG, Herder C, Rathmann W, et al. Prediabetes: a high-risk state for diabetes development[J]. Lancet, 2012, 379(9833): 2279-2290.

[17] Crujeiras AB, Diaz-Lagares A, Moreno-Navarrete JM, et al. Genome-wide DNA methylation pattern in visceral adipose tissue differentiates insulin-resistant from insulin-sensitive obese subjects[J]. Transl Res, 2016, 178: 13-24.e15.

[18] Muniandy M, Heinonen S, Yki-Jarvinen H, et al. Gene expression profile of subcutaneous adipose tissue in BMI-discordant monozygotic twin pairs unravels molecular and clinical changes associated with sub-types of obesity[J]. Int J Obes (Lond), 2017, 41(8): 1176-1184.

[19] Zhao J, Goldberg J, Bremner JD, et al. Global DNA methylation is associated with insulin resistance: a monozygotic twin study[J]. Diabetes, 2012, 61(2): 542-546.

[20] Simar D, Versteyhe S, Donkin I, et al. DNA methylation is altered in B and NK lymphocytes in obese and type 2 diabetic human[J]. Metabolism, 2014, 63(9): 1188-1197.

[21] Pietilainen KH, Ismail K, Jarvinen E, et al. DNA methylation and gene expression patterns in adipose tissue differ significantly within young adult monozygotic BMI-discordant twin pairs[J]. Int J Obes (Lond), 2016, 40(4): 654-661.

[22] Paneni F, Costantino S, Cosentino F. Role of oxidative stress in endothelial insulin resistance[J]. World J Diabetes, 2015, 6(2): 326-332.

[23] Gage MC, Yuldasheva NY, Viswambharan H, et al. Endothelium-specific insulin resistance leads to accelerated atherosclerosis in areas with disturbed flow patterns: a role for reactive oxygen species[J]. Atherosclerosis, 2013, 230(1): 131-139.

[24] Hasegawa Y, Saito T, Ogihara T, et al. Blockade of the nuclear factor-kappaB pathway in the endothelium prevents insulin resistance and prolongs life spans[J]. Circulation, 2012, 125(9): 1122-1133.

[25] Tabit CE, Shenouda SM, Holbrook M, et al. Protein kinase C-beta contributes to impaired endothelial insulin signaling in humans with diabetes mellitus[J]. Circulation, 2013, 127(1): 86-95.

[26] Costantino S, Paneni F, Virdis A, et al. Interplay among H3K9-editing enzymes SUV39H1, JMJD2C and SRC-1 drives p66Shc transcription and vascular oxidative stress in obesity[J]. Euro Heart J, 2019, 40(4): 383-391.

相似文献/References:

[1]张文珺 牛小伟 刘永铭.m6A甲基化在射血分数保留性心力衰竭中的作用的研究进展[J].心血管病学进展,2022,(1):44.[doi:10.16806/j.cnki.issn.1004-3934.2022.01.012]
 ZHANG Wenjun,NIU Xiaowei,LIU Yongming.m6A RNA Methylation in Heart Failure with Preserved Ejection Fraction[J].Advances in Cardiovascular Diseases,2022,(6):44.[doi:10.16806/j.cnki.issn.1004-3934.2022.01.012]
[2]傅义程 张福春 刘慧琳.表观遗传年龄与衰老和心血管疾病的研究进展[J].心血管病学进展,2022,(7):590.[doi:10.16806/j.cnki.issn.1004-3934.2022.07.000]
 FU Yicheng,ZHANG Fuchun,LIU Huilin.Epigenetic Age with Senescence and Cardiovascular Disease[J].Advances in Cardiovascular Diseases,2022,(6):590.[doi:10.16806/j.cnki.issn.1004-3934.2022.07.000]
[3]林力 陈敏 梁明露 宁璐璐 王紫 黄恺.非编码RNA在代谢性心血管疾病中的研究及治疗现状[J].心血管病学进展,2022,(10):915.[doi:10.16806/j.cnki.issn.1004-3934.2022.10.012]
 LIN Li,CHEN Min,LIANG Minglu,et al.Research and Treatment Status of Non-coding RNA in Metabolic Cardiovascular Disease[J].Advances in Cardiovascular Diseases,2022,(6):915.[doi:10.16806/j.cnki.issn.1004-3934.2022.10.012]
[4]郭梦阳 王守富 邢冬梅.DNA甲基化与原发性高血压关系研究进展[J].心血管病学进展,2023,(7):631.[doi:10.16806/j.cnki.issn.1004-3934.2023.07.013]
 GUO Mengyang,WANG Shoufu,XING Dongmei.Relationship Between DNA Methylation and Essential Hypertension[J].Advances in Cardiovascular Diseases,2023,(6):631.[doi:10.16806/j.cnki.issn.1004-3934.2023.07.013]
[5]刘娟婧,杨志明.白脂素对代谢性心血管疾病潜在作用的研究进展[J].心血管病学进展,2023,(8):728.[doi:10.16806/j.cnki.issn.1004-3934.2023.08.013]
 LIU Juanjing,YANG Zhiming.Effect of Asprosin on Metabolic Cardiovascular Disease[J].Advances in Cardiovascular Diseases,2023,(6):728.[doi:10.16806/j.cnki.issn.1004-3934.2023.08.013]

备注/Memo

备注/Memo:

通讯作者:许贞蓉,E-mail: xuzhenrong@xinhuamed.com?收稿日期:2019-03-30

更新日期/Last Update: 2019-12-16