Ablation of ALCAT1 mitigates hypertrophic cardiomyopathy through effects on oxidative stress and mitophagy

Molecular and Cellular Biology

Volumn 32, Issue 21, 2012, Pages 4493-4504

  Liu, Xiaolei ^a,b   Ye, Benlan ^b   Miller, Shane ^b   Yuan, Huijuan ^b   Zhang, Hongxiu ^b   Tian, Liang ^b   Nie, Jia ^b   Imae, Rieko ^c   Arai, Hiroyuki ^c   Li, Yuanjian ^a   Cheng, Zeneng ^a   Shi, Yuguang ^b  

^a CENTRAL SOUTH UNIVERSITY   (China)

^b PENN STATE COLLEGE OF MEDICINE   (United States)

^c UNIVERSITY OF TOKYO   (Japan)

Author keywords

[No Author keywords available]

Indexed keywords

ACYLTRANSFERASE; ALCAT1 ENZYME; CARDIOLIPIN; GUANOSINE TRIPHOSPHATASE; MAMMALIAN TARGET OF RAPAMYCIN; MITOCHONDRIAL DNA; PINK1 ENZYME; PROTEIN KINASE B; THYROID HORMONE; UNCLASSIFIED DRUG;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; AUTOPHAGY; CONTROLLED STUDY; DISORDERS OF MITOCHONDRIAL FUNCTIONS; ENZYME DEFICIENCY; HEART MUSCLE CELL; HYPERTHYROIDISM; HYPERTROPHIC CARDIOMYOPATHY; INSULIN RESISTANCE; LIPID PEROXIDATION; MALE; MITOPHAGY; MOUSE; NONHUMAN; OXIDATIVE STRESS; PRIORITY JOURNAL; SIGNAL TRANSDUCTION; UPREGULATION;

ACYLTRANSFERASES; ANIMALS; CARDIOLIPINS; CARDIOMYOPATHY, HYPERTROPHIC; CELL LINE; DNA, MITOCHONDRIAL; HEART FAILURE; MICE; MICE, KNOCKOUT; MITOCHONDRIA, HEART; MITOCHONDRIAL DEGRADATION; OXIDATIVE STRESS; PROTEIN KINASES; PROTO-ONCOGENE PROTEINS C-AKT; REACTIVE OXYGEN SPECIES; TOR SERINE-THREONINE KINASES; UP-REGULATION;

EID: 84868687470     PISSN: 02707306     EISSN: 10985549     Source Type: Journal    
DOI: 10.1128/MCB.01092-12     Document Type: Article

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