Ketty Schwartz, Jean-Jacques Mercadier
J Clin Invest.
2003;
112(5):652–654
doi:10.1172/JCI19632
This article Copyright © 2003, The American Society for Clinical Investigation
Abstract
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t has long been noted that while patients with familial hypertrophic cardiomyopathy due to cardiac troponin T (cTnT) mutations often suffer sudden cardiac death, they do not develop significant ventricular hypertrophy, suggesting that a distinct cellular mechanism apart from alterations in myocardial contractility is responsible. A new study has revealed that a single missense mutation in cTnT causes a striking disruption to energy metabolism, leading to cardiomyopathy.
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