Henan Key Laboratory of Medical Tissue Regeneration, Xinxiang Medical University, Xinxiang, China.
Cardiovascular Surgery, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China.
Exp Cell Res. 2024 Nov 1;443(1):114321. doi: 10.1016/j.yexcr.2024.114321. Epub 2024 Nov 5.
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.
缺血性心脏损伤会引发显著的炎症反应，激活并动员心肌成纤维细胞（CFs），最终导致心肌纤维化。在这项研究中，我们研究了钙激活氯离子通道（CaCC）蛋白 ANO1 在调节炎症条件下 CFs 迁移和黏附中的作用。我们的结果表明，ANO1 敲低显著减弱了 TGF-β和 IL-6 诱导的 CFs 黏附和迁移。这种抑制作用是通过下调整合素表达和减少粘着斑激酶（FAK）的激活来介导的，FAK 是细胞黏附和运动途径中的关键组成部分。这项研究为 CFs 迁移和黏附的机制提供了新的见解，并强调了 ANO1 作为治疗靶点的潜力，以减轻心肌梗死后的不良纤维化重塑。
