Epigenetics in Heart Failure

被引:0
作者
Ho, Jamie Sin Ying [1 ]
Jou, Eric [2 ,3 ]
Khong, Pek-Lan [4 ,5 ]
Foo, Roger S. Y. [1 ,6 ]
Sia, Ching-Hui [1 ,6 ]
机构
[1] Natl Univ Heart Ctr, Dept Cardiol, Singapore 119228, Singapore
[2] Univ Oxford, Dept Oncol, Oxford OX3 7DQ, England
[3] Univ Oxford, Kellogg Coll, Oxford OX2 6PN, England
[4] Natl Univ Hlth Syst, Natl Univ Hosp, Dept Diagnost Imaging, Singapore 119074, Singapore
[5] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Diagnost Radiol, Singapore 119074, Singapore
[6] Natl Univ Singapore, Yong Loo Lin Sch Med, Cardiovasc Res Inst, Singapore 117597, Singapore
基金
英国医学研究理事会;
关键词
heart failure; epigenetic modification; personalized medicine; histone modifications; DNA methylation; INDUCED CARDIAC-HYPERTROPHY; HISTONE-DEACETYLASE; DNA METHYLATION; GENE-EXPRESSION; CLASS-I; INHIBITION; STRESS; MATRIX-METALLOPROTEINASE-9; PHOSPHORYLATION; ASSOCIATION;
D O I
10.3390/ijms252212010
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Heart failure is a clinical syndrome with rising global incidence and poor prognosis despite improvements in medical therapy. There is increasing research interest in epigenetic therapies for heart failure. Pathological cardiac remodelling may be driven by stress-activated cardiac signalling cascades, and emerging research has shown the involvement of epigenetic signals that regulate transcriptional changes leading to heart failure. In this review, we appraise the current evidence for the role of epigenetic modifications in heart failure. These include DNA methylation and histone modifications by methylation, acetylation, phosphorylation, ubiquitination and sumoylation, which are critical processes that establish an epigenetic pattern and translate environmental stress into genetic expression, leading to cardiac remodeling. We summarize the potential epigenetic therapies currently in development, including the limited clinical trials of epigenetic therapies in heart failure. The dynamic changes in the epigenome in the disease process require further elucidation, and so does the impact of this process on the development of therapeutics. Understanding the role of epigenetics in heart failure may pave the way for the identification of novel biomarkers and molecular targets, and facilitate the development of personalized therapies for this important condition.
引用
收藏
页数:15
相关论文
共 75 条
[61]   The sirtuin SIRT6 blocks IGF-Akt signaling and development of cardiac hypertrophy by targeting c-Jun [J].
Sundaresan, Nagalingam R. ;
Vasudevan, Prabhakaran ;
Zhong, Lei ;
Kim, Gene ;
Samant, Sadhana ;
Parekh, Vishwas ;
Pillai, Vinodkumar B. ;
Ravindra, P. V. ;
Gupta, Madhu ;
Jeevanandam, Valluvan ;
Cunningham, John M. ;
Deng, Chu-Xia ;
Lombard, David B. ;
Mostoslavsky, Raul ;
Gupta, Mahesh P. .
NATURE MEDICINE, 2012, 18 (11) :1643-+
[62]   Trends in survival after a diagnosis of heart failure in the United Kingdom 2000-2017: population based cohort study [J].
Taylor, Clare J. ;
Ordonez-Mena, Jose M. ;
Roalfe, Andrea K. ;
Lay-Flurrie, Sarah ;
Jones, Nicholas R. ;
Marshall, Tom ;
Hobbs, F. D. Richard .
BMJ-BRITISH MEDICAL JOURNAL, 2019, 364
[63]   HDAC Inhibition Reverses Preexisting Diastolic Dysfunction and Blocks Covert Extracellular Matrix Remodeling [J].
Travers, Joshua G. ;
Wennersten, Sara A. ;
Pena, Brisa ;
Bagchi, Rushita A. ;
Smith, Harrison E. ;
Hirsch, Rachel A. ;
Vanderlinden, Lauren A. ;
Lin, Ying-Hsi ;
Dobrinskikh, Evgenia ;
Demos-Davies, Kimberly M. ;
Cavasin, Maria A. ;
Mestroni, Luisa ;
Steinkuhler, Christian ;
Lin, Charles Y. ;
Houser, Steven R. ;
Woulfe, Kathleen C. ;
Lam, Maggie P. Y. ;
McKinsey, Timothy A. .
CIRCULATION, 2021, 143 (19) :1874-1890
[64]   Hdac2 regulates the cardiac hypertrophic response by modulating Gsk3β activity [J].
Trivedi, Chinmay M. ;
Luo, Yang ;
Yin, Zhan ;
Zhang, Maozhen ;
Zhu, Wenting ;
Wang, Tao ;
Floss, Thomas ;
Goettlicher, Martin ;
Noppinger, Patricia Ruiz ;
Wurst, Wolfgang ;
Ferrari, Victor A. ;
Abrams, Charles S. ;
Gruber, Peter J. ;
Epstein, Jonathan A. .
NATURE MEDICINE, 2007, 13 (03) :324-331
[65]   The Epigenotype [J].
Waddington, C. H. .
INTERNATIONAL JOURNAL OF EPIDEMIOLOGY, 2012, 41 (01) :10-13
[66]   Matrix metalloproteinase-9 is a marker of heart failure after acute myocardial infarction [J].
Wagner, DR ;
Delagardelle, C ;
Ernens, I ;
Rouy, D ;
Vaillant, M ;
Beissel, J .
JOURNAL OF CARDIAC FAILURE, 2006, 12 (01) :66-72
[67]   Defective Sumoylation Pathway Directs Congenital Heart Disease [J].
Wang, Jun ;
Chen, Li ;
Wen, Shu ;
Zhu, Huiping ;
Yu, Wei ;
Moskowitz, Ivan P. ;
Shaw, Gary M. ;
Finnell, Richard H. ;
Schwartz, Robert J. .
BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY, 2011, 91 (06) :468-476
[68]   Epigenetic Therapy for the Treatment of Hypertension-Induced Cardiac Hypertrophy and Fibrosis [J].
Watson, Chris J. ;
Horgan, Stephen ;
Neary, Roisin ;
Glezeva, Nadezhda ;
Tea, Isaac ;
Corrigan, Niamh ;
McDonald, Ken ;
Ledwidge, Mark ;
Baugh, John .
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY AND THERAPEUTICS, 2016, 21 (01) :127-137
[69]   SIRT6 Mitigates Heart Failure With Preserved Ejection Fraction in Diabetes [J].
Wu, Xiaoqian ;
Liu, Huan ;
Brooks, Alan ;
Xu, Suowen ;
Luo, Jinque ;
Steiner, Rebbeca ;
Mickelsen, Deanne M. ;
Moravec, Christine S. ;
Jeffrey, Alexis D. ;
Small, Eric M. ;
Jin, Zheng Gen .
CIRCULATION RESEARCH, 2022, 131 (11) :926-943
[70]   Inhibition of DNA methylation reverses norepinephrine-induced cardiac hypertrophy in rats [J].
Xiao, DaLiao ;
Dasgupta, Chiranjib ;
Chen, Man ;
Zhang, Kangling ;
Buchholz, John ;
Xu, Zhice ;
Zhang, Lubo .
CARDIOVASCULAR RESEARCH, 2014, 101 (03) :373-382