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National Taiwan University Identifies N-Cadherin as a Key Regulator of Cardiac Regeneration, Published in Nature Communications

Heart failure affects 23 million people globally, with limited treatment options. Unlike adult human hearts, which lack regenerative capacity, neonatal hearts retain the ability to repair damage. A research team led by Professor Kai-Jen Yang at NTU’s Institute of Pharmacology discovered that N-Cadherin, a neural cadherin protein, plays a crucial role in cardiomyocyte proliferation and heart regeneration. Their study found that N-Cadherin levels are 2–3 times higher in neonatal cardiomyocytes than in adults and decline with age. Following heart injury, N-Cadherin expression increased, promoting cardiomyocyte proliferation. Loss of N-Cadherin reduced regeneration, while its overexpression reactivated cell cycling in adult mouse hearts, improving cardiac function post-myocardial infarction. Mechanistically, N-Cadherin binds to β-Catenin, stabilizing its protein levels and activating Wnt signaling, which regulates genes essential for cardiac repair. These findings suggest that modulating N-Cadherin could serve as a novel heart failure therapy.
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