The Pathogenesis of Cardiac Fibrosis: A Review of Recent Progress

Fibrosis is defined as the excessive deposition of extracellular matrix (ECM) proteins in the interstitium. It is an essential pathological response to chronic inflammation. ECM protein deposition is initially protective and is critical for wound healing and tissue regeneration. However, pathological cardiac remodeling in excessive and continuous tissue damage with subsequent ECM deposition results in a distorted organ architecture and significantly impacts cardiac function. In this review, we summarized and discussed the histologic features of cardiac fibrosis with the signaling factors that control it. We evaluated the origin and characteristic markers of cardiac fibroblasts. We also discussed lymphatic vessels, which have become more important in recent years to improve cardiac fibrosis.

Automated summary

Fibrosis is the excessive deposition of extracellular matrix (ECM) proteins in the interstitium, which is a pathological response to chronic inflammation. Although initially protective, excessive and continuous tissue damage and deposition lead to distorted organ structure and significant impact on cardiac function. This review summarizes the histologic features of cardiac fibrosis, the signaling factors that control it, the origin and characteristic markers of cardiac fibroblasts, and the growing importance of lymphatic vessels in improving cardiac fibrosis.