Beschreibung:
Activation and proliferation of cardiac fibroblasts are the prime mediators of cardiac fibrosis. Existing studies show that ROS and inflammatory cytokines produced during fibrosis not only signal proliferative stimuli but also contribute to DNA damage. Therefore, as a prerequisite to maintain sustained proliferation in fibroblasts, activation of distinct DNA repair mechanism is essential. We have previously shown a protective epigenetic role of TET3 in organ fibrosis. Here, we demonstrate that TET3 additionally impacts DNA damage response (DDR) mechanisms via orchestrating checkpoint-assist...