Extracellular matrix deposition and fibrosis pathway

The extracellular matrix deposition/fibrosis pathway refers to the interconnected set of processes and signaling events whereby ECM proteins, such as collagen, fibronectin, and hyaluronan, accumulate excessively within tissues during abnormal wound healing, resulting in fibrosis. Central mediators include myofibroblasts driven by signals such as TGF-β1, mechanical tension, and reciprocal ECM-cell interactions. Pathological ECM deposition changes tissue biomechanics, impairs organ function, and creates a "fibrogenic niche" that perpetuates disease. While no single molecule defines this pathway, therapeutic targets include signaling molecules that regulate ECM production (e.g., TGF-β1) and enzymes mediating ECM remodeling (e.g., matrix metalloproteinases), with several approved and experimental antifibrotic agents aiming to prevent, reverse, or resolve fibrosis by modulating ECM synthesis and breakdown[1][2][3][4][5][7]. This entry describes a process, not a canonical molecule or receptor, and should not be used as a direct therapeutic target entry. For drug development or structured information, focus on molecular targets within the pathway (e.g., TGF-β1, collagen, matrix metalloproteinases)[1][2][4][7].

Other names

Fibrosis pathwayECM deposition pathwayTissue fibrosis signalingFibrogenesis pathway

Inhibition of pro-fibrotic cytokines (e.g., TGF-β1) Inhibition of ECM synthesis Promotion of ECM degradation/remodeling Blockade of myofibroblast differentiation