Genetic deficiency of PAI-1 in aged mice promotes cardiac fibrosis, potentially linking endothelial-to-mesenchymal transition and TGF-β signaling.
These results indicate that spontaneous activation of both Smad and non-Smad transforming growth factor-β signaling may contribute to profibrotic responses in aged PAI-1-deficient mice hearts and establish a possible link between endothelial-to-mesenchymal transition and cardiac fibrosis in PAI-1-deficient mice.
Ghosh et al. (Wed,) studied this question.