Genetic deficiency of plasminogen activator inhibitor-1 promotes cardiac fibrosis in aged mice: involvement of constitutive transforming growth factor-beta signaling and endothelial-to-mesenchymal transition.

@article{Ghosh2010GeneticDO,
  title={Genetic deficiency of plasminogen activator inhibitor-1 promotes cardiac fibrosis in aged mice: involvement of constitutive transforming growth factor-beta signaling and endothelial-to-mesenchymal transition.},
  author={Asish Kumar Ghosh and William S. Bradham and Linda A. Gleaves and Bart De Taeye and Sheila B. Murphy and Joseph W. Covington and Douglas E. Vaughan},
  journal={Circulation},
  year={2010},
  volume={122 12},
  pages={1200-9}
}
BACKGROUND Elevated levels of plasminogen activator inhibitor-1 (PAI-1), a potent inhibitor of urokinase plasminogen activator and tissue plasminogen activator, are implicated in the pathogenesis of tissue fibrosis. Paradoxically, lack of PAI-1 in the heart is associated with the development of cardiac fibrosis in aged mice. However, the molecular basis of cardiac fibrosis in aged PAI-1-deficient mice is unknown. Here, we investigated the molecular and cellular bases of myocardial fibrosis… CONTINUE READING

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