Excessive collagen type VII mediates pleural fibrosis via increasing extracellular matrix stiffness

Cell extracellular matrix interactions are critical in fibrosis. We found that collagen type VII, an ECM component essential for cell anchoring, was upregulated in pleural tissue of patients with tuberculous pleural fibrosis. In cellular and animal models, collagen VII increased at early stages of fibrosis, preceding collagen I and ACTA2. Mesothelial cell specific deletion of collagen VII attenuated experimental pleural fibrosis in mice. These findings indicate that excessive collagen VII promotes pleural fibrosis by increasing ECM stiffness.