Epigenetic alterations of TGFβ and its main canonical signaling mediators in the context of cardiac fibrosis

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.
This work was supported by the Agencia Estatal de Investigación, Spain (RTI2018-095214-B-I00; and BIO2015-72124-EXP), and the IDIVAL InnVal 17/22, NextVal 18/11 Thanks to the University of Cantabria and the IDIVAL (UC-IDIVAL Fellows program; grant number PREVAL19/05: Maestro D and UC: Algeciras L) for financial support.