Fig. 1
From: An extracellular matrix paradox in myocardial scar formation
When less becomes more: Col V depletion results in a paradoxical increase in scar size post-MI. Type V collagen (Col V)-deficient mouse hearts subjected to experimental myocardial infarction (MI) exhibit increased scar size post-injury, with altered mechanical and structural properties. Col V-deficient fibroblasts exhibit elevated expression of integrins αVβ3 and αVβ5, which promote myofibroblast differentiation and could result from either a cell-intrinsic compensatory activation of pro-fibrotic gene programs, or b a feedback loop characterized by cell-extrinsic mechanosensitive upregulation, or both. Cilengitide, a specific inhibitor of αVβ3 and αVβ5 integrins, rescues the phenotype and suggests integrin-dependent signaling as a potential target for anti-fibrotic therapeutics
