[Molecular and cellular mechanisms of organ fibrosis]

Extracellular matrix (ECM) is important component for the organ architecture and function, and dynamically regulated by fibroblasts in normal state. In pathological condition, abnormal ECM accumulation or fibrosis is induced by pathological stimulation and associated with organ dysfunction in liver, lung, kidney and heart. In the process of fibrosis, complex molecular mechanisms including renin-angiotensin-aldosterone system and transforming growth factor beta signaling play critical roles regulating fibroblast activation and ECM deposition. In addition to resident fibroblasts, it has been reported that other cell types originated from epithelial/endothelial mesenchymal transition, circulating fibrocytes, or pericytes also contribute to fibrosis. Detailed examination for molecular and cellular mechanisms of fibrosis can contribute to future therapy for organ failure.