期刊
SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
卷 97, 期 -, 页码 26-37出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.semcdb.2019.04.009
关键词
Myocardial infarction; Cardiac regeneration; Epigenetic; Chromatin dynamics; microRNA; Methylation; Deacetylation
资金
- Spanish Ministry of Economy and Competitiveness-MINECO [SAF2017-84324-C2-1-R]
- Instituto de Salud Carlos III [PI17/01487, PIC18/0014]
- Red de Terapia Celular - TerCel [RD16/0011/0006]
- CIBER Cardiovascular projects, as part of the Plan Nacional de I + D + I [CB16/11/00403]
- ISCIII-Sudireccion General de Evaluacion y el Fondo Europeo de Desarrollo Regional [FEDER]
- Fundacio La MARATO de TV3 [201516-10, 201502-20]
- Generalitat de Catalunya [SGR2017 00483, SLT002/16/00234]
- CERCA Programme/Generalitat de Catalunya
- Societat Catalana de Cardiologia
- la Caixa Banking Foundation
- ACCIO [Catalonia Trade Investment
- Generalitat de Catalunya] under the Catalonian ERDF [European Regional Development Fund] operational program [2014-2020]
Heart failure of ischemic origin is caused by the presence of a large scar resulting from an acute myocardial infarction. Acute myocardial infarction generally occurs when blood supply to the heart is blocked. Regenerative strategies that limit infarct injury would be able to prevent adverse post-ischemic remodelling and maintain the structural support necessary for effective cardiomyocyte contraction. Our understanding of endogenous cardiac regeneration and its biology has exposed a variety of targets for therapeutic approaches, such as non-coding RNAs, DNA methylation, histone modifications, direct cardiac reprogramming, cell transplantation, stimulation of resident cardiomyocytes, proliferation, and inhibition of cardiomyocyte death. In this review, we address the epigenetic mechanisms underlying these strategies and the use of therapeutic epigenetic molecules or epidrugs.
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