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Abstract
Fatty acids are the most major substrate source for adult cardiac energy generation. Prohibitin 2 (PHB2), a highly conserved protein located in mitochondrial inner membrane, plays key roles in cellular energy metabolic homeostasis. However, its functions in regulating cardiac fatty acid metabolism have remained largely unknown. Our study demonstrates that cardiac-specific knockout of Phb2 leads to accumulation of lipid droplets and causes heart failure. Mechanistically, ablation of PHB2 impairs cardiac fatty acid oxidation (FAO) through downregulating carnitine palmitoyltransferase1b (CPT1b), a rate-limiting enzyme of cardiac mitochondrial FAO. Moreover, overexpression of CPT1b alleviates impaired FAO in PHB2-deficient cardiomyocytes. Thus, our study provides direct evidence for the link between PHB2 and cardiac fatty acid metabolism. Our study points out that PHB2 is a potential FAO regulator in cardiac mitochondrial inner membrane, as well as the connection between PHB2 and CPT1b and their relationships to cardiac pathology especially to cardiac fatty acid metabolic disorder.
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1 Peking University, State Key Laboratory of Membrane Biology, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking-Tsinghua Center for Life Sciences, Institute of Molecular Medicine, Beijing, China (GRID:grid.11135.37) (ISNI:0000 0001 2256 9319); Sun Yat-sen University, State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Guangzhou, China (GRID:grid.12981.33) (ISNI:0000 0001 2360 039X)
2 Peking University, State Key Laboratory of Membrane Biology, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking-Tsinghua Center for Life Sciences, Institute of Molecular Medicine, Beijing, China (GRID:grid.11135.37) (ISNI:0000 0001 2256 9319)
3 Sun Yat-sen University, State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Guangzhou, China (GRID:grid.12981.33) (ISNI:0000 0001 2360 039X)