PMID- 29902536
OWN - NLM
STAT- MEDLINE
DCOM- 20190916
LR  - 20211204
IS  - 1090-2422 (Electronic)
IS  - 0014-4827 (Linking)
VI  - 370
IP  - 1
DP  - 2018 Sep 1
TI  - Aldolase promotes the development of cardiac hypertrophy by targeting AMPK 
      signaling.
PG  - 78-86
LID - S0014-4827(18)30339-2 [pii]
LID - 10.1016/j.yexcr.2018.06.009 [doi]
AB  - 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.
CI  - Copyright (c) 2018 Elsevier Inc. All rights reserved.
FAU - Li, Yapeng
AU  - Li Y
AD  - Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, 
      Zhengzhou, China.
FAU - Zhang, Dianhong
AU  - Zhang D
AD  - Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, 
      Zhengzhou, China.
FAU - Kong, Lingyao
AU  - Kong L
AD  - Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, 
      Zhengzhou, China.
FAU - Shi, Huiting
AU  - Shi H
AD  - Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, 
      Zhengzhou, China.
FAU - Tian, Xinyu
AU  - Tian X
AD  - Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, 
      Zhengzhou, China.
FAU - Gao, Lu
AU  - Gao L
AD  - Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, 
      Zhengzhou, China.
FAU - Liu, Yuzhou
AU  - Liu Y
AD  - Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, 
      Zhengzhou, China.
FAU - Wu, Leiming
AU  - Wu L
AD  - Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, 
      Zhengzhou, China.
FAU - Du, Binbin
AU  - Du B
AD  - Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, 
      Zhengzhou, China.
FAU - Huang, Zhen
AU  - Huang Z
AD  - Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, 
      Zhengzhou, China.
FAU - Liang, Cui
AU  - Liang C
AD  - Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, 
      Zhengzhou, China.
FAU - Wang, Zheng
AU  - Wang Z
AD  - Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, 
      Zhengzhou, China.
FAU - Yao, Rui
AU  - Yao R
AD  - Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, 
      Zhengzhou, China.
FAU - Zhang, Yanzhou
AU  - Zhang Y
AD  - Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, 
      Zhengzhou, China. Electronic address: zhangyzxnk@163.com.
LA  - eng
PT  - Journal Article
DEP - 20180611
PL  - United States
TA  - Exp Cell Res
JT  - Experimental cell research
JID - 0373226
RN  - 0 (Ribonucleotides)
RN  - 360-97-4 (Aminoimidazole Carboxamide)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
RN  - EC 4.1.2.13 (Fructose-Bisphosphate Aldolase)
RN  - F0X88YW0YK (AICA ribonucleotide)
SB  - IM
MH  - AMP-Activated Protein Kinases/*metabolism
MH  - Aminoimidazole Carboxamide/analogs & derivatives/metabolism
MH  - Animals
MH  - Cardiomegaly/*metabolism/*pathology
MH  - Fructose-Bisphosphate Aldolase/*metabolism
MH  - Heart/physiopathology
MH  - Heart Failure/metabolism/pathology
MH  - Male
MH  - Mice
MH  - Myocardium/metabolism/pathology
MH  - Myocytes, Cardiac/metabolism/pathology
MH  - Protein Serine-Threonine Kinases/metabolism
MH  - Ribonucleotides/metabolism
MH  - Signal Transduction/*physiology
MH  - Up-Regulation/physiology
OTO - NOTNLM
OT  - AMPK
OT  - Aldolase A
OT  - Cardiac hypertrophy
OT  - LKB1
OT  - Metabolism
EDAT- 2018/06/15 06:00
MHDA- 2019/09/17 06:00
CRDT- 2018/06/15 06:00
PHST- 2018/02/03 00:00 [received]
PHST- 2018/05/27 00:00 [revised]
PHST- 2018/06/10 00:00 [accepted]
PHST- 2018/06/15 06:00 [pubmed]
PHST- 2019/09/17 06:00 [medline]
PHST- 2018/06/15 06:00 [entrez]
AID - S0014-4827(18)30339-2 [pii]
AID - 10.1016/j.yexcr.2018.06.009 [doi]
PST - ppublish
SO  - Exp Cell Res. 2018 Sep 1;370(1):78-86. doi: 10.1016/j.yexcr.2018.06.009. Epub 
      2018 Jun 11.