TGFB1 and Myocardial fibrosis: When the autophagy inhibitors 3-methyladenine or chloroquine (CQ)were used to block autophagy, collagen secretion was significantly reduced,suggesting that activated autophagy may promote myocardial fibrosis [40].Homoplastically, primary human atrial myofibroblasts were treated withTGF-β1 to assess fibrogenic and autophagic responses.The results showed that TGF-β1 led to an elevation ofautophagic markers and fibronectin, and pharmacological inhibition of autophagydecreased the fibrotic response, these results support that TGFβ1-inducedautophagy increases the fibrogenetic response [41].