Figure 9. Schematic model showing the mechanistic pathway by which TRPV4 mediates myofibroblast differentiation and pulmonary fibrosis.

Our data suggest that TRPV4-dependent Ca²⁺ influx activity is sensitized by stiff matrices within the pathophysiological range. Interaction between TRPV4 activity (Ca²⁺ influx) and the profibrotic TGF-β1 signals promote nuclear localization of α-SMA transcription factor, MRTF-A, via regulation of actomyosin remodeling to potentiate myofibroblast differentiation during fibrogenesis. TβR, TGF-βR.