The role of the bidirectional regulatory network between immune cells and stromal cells in cardiac repair and fibrosis following myocardial infarction.

Heart failure following myocardial infarction (MI) is a major complication affecting long-term prognosis of patient, with its core pathological processes being ventricular pathological remodeling and fibrosis. This process is not merely simple scar formation, but is dominated by a continuous, dynamic, and intricate bidirectional dialogue between immune cells and cardiac stromal cells. This review systematically mapped the complex interactive networks between immune cells-including neutrophils, macrophages, and lymphocytes-and stromal cells such as cardiac fibroblasts, endothelial cells, and pericytes during the spatiotemporal evolution following MI. We emphasizes the key communication pathways involving cytokines, chemokines, fibrotic signals, and active signals from the microenvironment. And we mappied their spatiotemporal network governing the initiation and resolution of inflammation and fibrosis. Simultaneously, we explored how this network's imbalance shifts from essential repair responses to pathological fibrosis, ultimately leading to heart failure. Furthermore, we summarized novel therapeutic strategies targeting the immune-matrix axis, aiming to provide new perspectives and theoretical foundations for the precise prevention and treatment of heart failure following MI.