1. Epigenetic alterations of TGFβ and its main canonical signaling mediators in the context of cardiac fibrosis.
- Author
-
Algeciras, Luis, Palanca, Ana, Maestro, David, RuizdelRio, Jorge, and Villar, Ana V.
- Subjects
- *
HEART fibrosis , *TRANSFORMING growth factors , *HISTONE methyltransferases , *EPIGENETICS , *HEART injuries - Abstract
Cardiac fibrosis is a pathological process that presents a continuous overproduction of extracellular matrix (ECM) components in the myocardium, which negatively influences the progression of many cardiac diseases. Transforming growth factor β (TGFβ) is the main ligand that triggers the production of pro-fibrotic ECM proteins. In the cardiac fibrotic process, TGFβ and its canonical signaling mediators are tightly regulated at different levels as well as epigenetically. Cardiac fibroblasts are one of the most important TGFβ target cells activated after cardiac injury. TGFβ-driven fibroblast activation is subject to epigenetic modulation and contributes to the progression of cardiac fibrosis, mainly through the expression of pro-fibrotic molecules implicated in the disease. In this review, we describe epigenetic regulation related to canonical TGFβ signaling in cardiac fibroblasts. [Display omitted] • Cardiac fibrosis includes the TGFβ-related epigenetic regulation in fibroblasts. • Modulation of DNA and histone methyltransferases alters TGFβ-mediated signaling. • Modulation of histone deacetylases alters TGFβ-mediated signaling. • NcRNAs generate a regulatory network that controls TGFβ-dependent cardiac fibrosis. • Classical epigenetic regulators and ncRNAs interconnect to control cardiac fibrosis. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF