Piezo1 Knockdown Activates PI3K/AKT and Enhances SPP1 to Drive M2 Macrophage Polarization and Reduce Cardiac Inflammation
We have successfully established a mouse model with myeloid cell-specific knockdown of Piezo1.   The intraperitoneal injection of lipopolysaccharide (LPS) resulted in a significant increase in cardiac macrophage infiltration, as well as an increase in the expression of inflammatory factors and the inflammatory response.   However, myeloid cell-specific knockdown of Piezo1 impaired this response, leading to an increase in macrophage polarization towards the M2 type and the decreased inflammatory response.   As a result, myocardial injury caused by sepsis was attenuated.   We have also demonstrated that the PI3K/AKT pathway is significantly activated after Piezo1 knockdown, resulting in reduced myocardial dysfunction. Overall design: RNA-sequencing profiling of macrophages from Piezo1^flox/flox and Piezo1^flox/flox Lyz2-Cre C57BL/6J mice following lipopolysaccharide (LPS) treatment.