Knockdown of ANO1 decreases TGF-β- and IL-6-induced adhesion and migration of cardiac fibroblasts by inhibiting the expression of integrin and focal adhesion kinase.

Ischemic cardiac injury triggers a significant inflammatory response, activating and mobilizing cardiac fibroblasts (CFs), which ultimately contributes to myocardial fibrosis. In this study, we investigated the role of ANO1, a calcium-activated chloride channel (CaCC) protein, in regulating CFs migration and adhesion under inflammatory conditions. Our results demonstrated that ANO1 knockdown significantly attenuated TGF-β- and IL-6-induced adhesion and migration of CFs. This inhibitory effect was mediated through the downregulation of integrin expression and reduced activation of focal adhesion kinase (FAK), key components in cellular adhesion and motility pathways. This study provides new insights into the mechanisms underlying CFs migration and adhesion, highlighting the potential of ANO1 as a therapeutic target for mitigating adverse fibrotic remodeling following myocardial infarction.