Inhibition of Pin1 alleviates myocardial fibrosis and dysfunction in STZ-induced diabetic mice

In diabetic mice, cardiac Pin1 levels, TGF-β1, and collagen deposits are increased, but these changes are effectively prevented by Pin1 inhibition.

• Cardiac fibrosis and dysfunction in diabetic mice are linked to increased levels of Pin1.
• Inhibition of Pin1 using juglone reduces cardiac fibrosis and improves cardiac function.
• High glucose conditions elevate Pin1 expression and activate several signaling pathways in cardiac fibroblasts.
• Pin1 inhibition prevents the increase in key proteins associated with fibrosis in cardiac fibroblasts.
• Inhibition of Pin1 also reduces the proliferation and migration of cardiac fibroblasts induced by high glucose.

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