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Aldolase promotes the development of cardiac hypertrophy by targeting AMPK signaling.
Li, Yapeng; Zhang, Dianhong; Kong, Lingyao; Shi, Huiting; Tian, Xinyu; Gao, Lu; Liu, Yuzhou; Wu, Leiming; Du, Binbin; Huang, Zhen; Liang, Cui; Wang, Zheng; Yao, Rui; Zhang, Yanzhou.
Afiliação
  • Li Y; Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
  • Zhang D; Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
  • Kong L; Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
  • Shi H; Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
  • Tian X; Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
  • Gao L; Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
  • Liu Y; Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
  • Wu L; Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
  • Du B; Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
  • Huang Z; Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
  • Liang C; Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
  • Wang Z; Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
  • Yao R; Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
  • Zhang Y; Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. Electronic address: zhangyzxnk@163.com.
Exp Cell Res ; 370(1): 78-86, 2018 09 01.
Article em En | MEDLINE | ID: mdl-29902536
Metabolic dysfunction is a hallmark of cardiac hypertrophy and heart failure. During cardiac failure, the metabolism of cardiomyocyte switches from fatty acid oxidation to glycolysis. However, the roles of key metabolic enzymes in cardiac hypertrophy are not understood fully. Here in the present work, we identified Aldolase A (AldoA) as a core regulator of cardiac hypertrophy. The mRNA and protein levels of AldoA were significantly up-regulated in transverse aortic constriction (TAC)- and isoproterenol (ISO)-induced hypertrophic mouse hearts. Overexpression of AldoA in cardiomyocytes promoted ISO-induced cardiomyocyte hypertrophy, whereas AldoA knockdown repressed cardiomyocyte hypertrophy. In addition, adeno-associated virus 9 (AAV9)-mediated in vivo knockdown of AldoA in the hearts rescued ISO-induced decrease in cardiac ejection fraction and fractional shortening and repressed cardiac hypertrophy. Mechanism study revealed that AldoA repressed the activation of AMP-dependent protein kinase (AMPK) signaling in a liver kinase B1 (LKB1)-dependent and AMP-independent manner. Inactivation of AMPK is a core mechanism underlying AldoA-mediated promotion of ISO-induced cardiomyocyte hypertrophy. By contrast, activation of AMPK with metformin and AICAR blocked AldoA function during cardiomyocyte hypertrophy. In summary, our data support the notion that AldoA-AMPK axis is a core regulatory signaling sensing energetic status and participates in cardiac hypertrophy.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Transdução de Sinais / Cardiomegalia / Proteínas Quinases Ativadas por AMP / Frutose-Bifosfato Aldolase Limite: Animals Idioma: En Revista: Exp Cell Res Ano de publicação: 2018 Tipo de documento: Article País de afiliação: China

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Transdução de Sinais / Cardiomegalia / Proteínas Quinases Ativadas por AMP / Frutose-Bifosfato Aldolase Limite: Animals Idioma: En Revista: Exp Cell Res Ano de publicação: 2018 Tipo de documento: Article País de afiliação: China