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.