In summary, the TREM-1–PI3 K/AKT–FoxO3a pathway maintains a chronic inflammatory microenvironment in cardiac tissue by enhancing pro-inflammatory gene expression, downregulating anti-inflammatory signaling activity, and promoting immune cell recruitment in cardiac pathological states, which may provide a mechanistic basis for myocardial inflammation and fibrosis in diseases such as atrial fibrillation. The gene discussed is TREM1; the disease is atrial fibrillation.