Unraveling Fibrosis: Mechanisms, Clinical Impact, and Therapeutic Frontiers

Fibrosis is a pathological process characterized by the excessive accumulation of extracellular matrix (ECM) components, particularly collagen, leading to tissue stiffening, scarring, and loss of normal organ function. It often develops as a maladaptive response to chronic injury, inflammation, or stress, when normal wound-healing mechanisms become dysregulated and persist. Activated fibroblasts and myofibroblasts play central roles by secreting ECM proteins and growth factors, while signaling pathways such as TGF-β, Wnt, and NF-κB drive the fibrotic response. Fibrosis can occur in multiple organs including the heart, lungs, liver, and kidneys and is a hallmark of many chronic diseases such as heart failure, pulmonary fibrosis, cirrhosis, and chronic kidney disease. Despite its prevalence and impact on morbidity and mortality, effective antifibrotic therapies remain limited, making the study of fibrosis a critical focus in translational medicine and regenerative research.