Carnitine Palmitoyltransferase-1b Deficiency Aggravates Pressure Overload–Induced Cardiac Hypertrophy Caused by Lipotoxicity
Author(s) -
Lan He,
Teayoun Kim,
Qinqiang Long,
Jian Liu,
Peiyong Wang,
Yiqun Zhou,
Yishu Ding,
Jeevan K. Prasain,
Philip A. Wood,
Qinglin Yang
Publication year - 2012
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.111.075978
Subject(s) - pressure overload , medicine , endocrinology , lipotoxicity , heart failure , muscle hypertrophy , cardiac hypertrophy , insulin resistance , insulin
Carnitine palmitoyltransferase-1 (CPT1) is a rate-limiting step of mitochondrial β-oxidation by controlling the mitochondrial uptake of long-chain acyl-CoAs. The muscle isoform, CPT1b, is the predominant isoform expressed in the heart. It has been suggested that inhibiting CPT1 activity by specific CPT1 inhibitors exerts protective effects against cardiac hypertrophy and heart failure. However, clinical and animal studies have shown mixed results, thereby creating concerns about the safety of this class of drugs. Preclinical studies using genetically modified animal models should provide a better understanding of targeting CPT1 to evaluate it as a safe and effective therapeutic approach.
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