PMID- 34594408
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211002
IS  - 1792-1015 (Electronic)
IS  - 1792-0981 (Print)
IS  - 1792-0981 (Linking)
VI  - 22
IP  - 5
DP  - 2021 Nov
TI  - TFEC contributes to cardiac hypertrophy by inhibiting AMPK/mTOR signaling.
PG  - 1271
LID - 10.3892/etm.2021.10706 [doi]
LID - 1271
AB  - The underlying mechanism of cardiac hypertrophy has not yet been fully 
      elucidated. The present study aimed to explore the function of transcription 
      factor EC (TFEC) in mouse models of cardiac hypertrophy and to determine the 
      underlying mechanism. Pressure-overload cardiac hypertrophy and angiotensin II 
      (AngII) infusion-induced animal models of cardiac hypertrophy were established in 
      vivo. The expression of TFEC was explored via western blotting. The results 
      demonstrated that TFEC expression was significantly increased in the hearts of 
      mice with pressure overload- and AngII-induced hypertrophy. Injection of 
      rAd-short hairpin (sh)-TFEC significantly decreased the expression of TFEC in 
      heart tissues compared with group injected with rAd-negative control (NC). 
      Furthermore, the expression levels of atrial natriuretic peptide (ANP), brain 
      natriuretic peptide (BNP) and beta-myosin heavy chain (beta-MHC) were increased in the 
      hearts of AngII-treated mice; however, compared with rAd-NC transfection, 
      transfection with rAd-sh-TFEC decreased the expression levels of ANP, BNP and 
      beta-MHC. The results from echocardiographic analysis indicated that transfection 
      with rAd-sh-TFEC improved the cardiac function of AngII-treated mice compared 
      with transfection with rAd-NC. In addition, the AngII-induced increase in 
      cardiomyocyte size could be reversed by TFEC knockdown in primary cardiomyocytes. 
      The elevated expression levels of ANP, BNP and beta-MHC induced by AngII could be 
      partially abolished following TFEC knockdown. The results from western blotting 
      demonstrated that TFEC overexpression decreased the expression of phosphorylated 
      AMP-activated protein kinase (AMPK)/acetyl-CoA carboxylase (ACC) but increased 
      the expression of phosphorylated mechanistic target of rapamycin (mTOR). 
      Furthermore, Compound C significantly suppressed the activation of AMPK/ACC but 
      increased the activation of mTOR, even in primary cardiomyocytes transfected with 
      rAd-sh-TFEC. In conclusion, the findings from this study demonstrated that TFEC 
      was overexpressed in the hearts of mice with cardiac hypertrophy and that 
      silencing TFEC may improve AngII-induced cardiac hypertrophy and dysfunction by 
      activating AMPK/mTOR signaling.
CI  - Copyright: (c) Zhao et al.
FAU - Zhao, Ting
AU  - Zhao T
AD  - Department of Cardiology, Weapon Industry 521 Hospital, Xi'an, Shanxi 710065, 
      P.R. China.
FAU - Wang, Zhenyu
AU  - Wang Z
AD  - Department of Cardiology, Weapon Industry 521 Hospital, Xi'an, Shanxi 710065, 
      P.R. China.
FAU - Chi, Yehong
AU  - Chi Y
AD  - Department of Cardiology, Weapon Industry 521 Hospital, Xi'an, Shanxi 710065, 
      P.R. China.
FAU - Ni, Chunmei
AU  - Ni C
AD  - Department of Cardiology, Weapon Industry 521 Hospital, Xi'an, Shanxi 710065, 
      P.R. China.
FAU - Zheng, Xudan
AU  - Zheng X
AD  - Department of Cardiology, Weapon Industry 521 Hospital, Xi'an, Shanxi 710065, 
      P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20210907
PL  - Greece
TA  - Exp Ther Med
JT  - Experimental and therapeutic medicine
JID - 101531947
PMC - PMC8456502
OTO - NOTNLM
OT  - AMP-activated protein kinase/mechanistic target of rapamycin signaling
OT  - cardiac hypertrophy
OT  - kinase non-catalytic C-lobe domain containing 1
COIS- The authors declare that they have no competing interests.
EDAT- 2021/10/02 06:00
MHDA- 2021/10/02 06:01
PMCR- 2021/09/07
CRDT- 2021/10/01 07:27
PHST- 2021/04/08 00:00 [received]
PHST- 2021/07/09 00:00 [accepted]
PHST- 2021/10/01 07:27 [entrez]
PHST- 2021/10/02 06:00 [pubmed]
PHST- 2021/10/02 06:01 [medline]
PHST- 2021/09/07 00:00 [pmc-release]
AID - ETM-22-5-10706 [pii]
AID - 10.3892/etm.2021.10706 [doi]
PST - ppublish
SO  - Exp Ther Med. 2021 Nov;22(5):1271. doi: 10.3892/etm.2021.10706. Epub 2021 Sep 7.