By contrast, the inhibition of Pin1 alleviated cardiac damage and fibrosis in the experimental models, suggesting that Pin1 contributed to the development of cardiac remodeling in ISO‑administered rats, and that the inactivation of Pin1 may be a novel therapeutic candidate for the treatment of cardiovascular disease and heart failure.
On the basis of these findings, the aim of this study is to define Pin1 as a novel modulator of Ca<sup>2+</sup> handling, with implications for improving myocardial contractility and potential for ameliorating development of heart failure.
Here, we show that either genetic deletion or cardiac overexpression of Pin1 blunts hypertrophic responses induced by transaortic constriction and consequent cardiac failure in vivo.