Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10815426 | Cellular Signalling | 2013 | 7 Pages |
Abstract
Cardiac fibrosis is characterized by excessive extracellular matrix accumulation that ultimately destroys tissue architecture and eventually abolishes normal function. In recent years, despite the underlying mechanisms of cardiac fibrosis are still unknown, numerous studies suggest that epigenetic modifications impact on the development of cardiac fibrosis. Epigenetic modifications control cell proliferation, differentiation, migration, and so on. Epigenetic modifications contain three main processes: DNA methylation, histone modifications, and silencing by microRNAs. We here outline the recent work pertaining to epigenetic changes in cardiac fibrosis. This review focuses on the epigenetic regulation of cardiac fibrosis.
Keywords
PI3Kinsulin-like growth factor-II receptorIGF-IIRAngiotension IIECMshMTDNA methyltransferases5-Aza-dCEZH2DNMTsPPARγHDACERKα-SMAMMPTGF-β1TSA5-Aza-2′-deoxycytidineMAPKEpigeneticsα-smooth muscle actinTransforming growth factor-β1Trichostatin AHistone modificationsenhancer of zeste homolog 2Ang-IImicroRNAsTIMPCardiac fibrosisExtracellular matrixmatrix metalloproteinaseDNA methylationTissue inhibitor of metalloproteinaseMicroRNAMiRNAhistone deacetylasesHistone acetyltransferaseHistone Methyltransferasemitogen-activated protein kinaseHATextracellular signal-regulated kinaseperoxisome proliferator-activated receptor γ
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Authors
Hui Tao, Kai-Hu Shi, Jing-Jing Yang, Cheng Huang, Li-Ping Liu, Jun Li,