PMID- 34468254
OWN - NLM
STAT- MEDLINE
DCOM- 20211222
LR  - 20231213
IS  - 2165-5987 (Electronic)
IS  - 2165-5979 (Print)
IS  - 2165-5979 (Linking)
VI  - 12
IP  - 1
DP  - 2021 Dec
TI  - Circ_nuclear factor I X (circNfix) attenuates pressure overload-induced cardiac 
      hypertrophy via regulating miR-145-5p/ATF3 axis.
PG  - 5373-5385
LID - 10.1080/21655979.2021.1960462 [doi]
AB  - Cardiac hypertrophy can cause heart failure. However, the mechanisms underlying 
      the progression of cardiac hypertrophy remain unclear. Emerging evidence suggests 
      that circular RNAs (circRNAs) play a critical role in cardiac hypertrophy. 
      However, the association between circ_nuclear factor I X (circNfix) and cardiac 
      hypertrophy remain largely unknown. Therefore, the aim of the present study was 
      to explore the role of circNfix in cardiac hypertrophy. In order to detect the 
      function of circNfix in cardiac hypertrophy, cardiomyocytes were stimulated with 
      angiotensin II (Ang II) to mimic the pathogenesis of the disease. In addition, 
      pressure overload-induced cardiac hypertrophy in a mouse model was established 
      using transverse aortic constriction (TAC) surgery. The mechanism via which 
      circNfix regulated cardiac hypertrophy was investigated using RNA pull-down and 
      luciferase reporter assays, and fluorescence in situ hybridization (FISH). 
      circNfix was downregulated in Ang II-treated cardiomyocytes. Similarly, circNfix 
      expression was markedly downregulated in mice following TAC surgery. In addition, 
      circNfix overexpression significantly prevented the progression of cardiac 
      hypertrophy in TAC-treated mice. Luciferase activity and RNA pull-down assays 
      indicated that circNfix could indirectly target activating transcription factor 3 
      (ATF3) by binding with microRNA (miR)-145-5p in cardiomyocytes. miR-145-5p 
      overexpression or ATF3 knockdown could reverse the effects of circNfix in Ang 
      II-treated mouse cardiomyocytes. circNfix attenuated pressure overload-induced 
      cardiac hypertrophy by regulating the miR-145-5p/ATF3 axis. Therefore, circNfix 
      may serve as a molecular target for cardiac hypertrophy treatment.
FAU - Pan, Jun
AU  - Pan J
AD  - Department of Thoracic and Cardiovascular Surgery, The Affiliated Drum Tower 
      Hospital of Nanjing University Medical School, Nanjing, Jiangsu, China.
FAU - Xu, Zhenjun
AU  - Xu Z
AD  - Department of Thoracic and Cardiovascular Surgery, The Affiliated Drum Tower 
      Hospital of Nanjing University Medical School, Nanjing, Jiangsu, China.
FAU - Guo, Guanjun
AU  - Guo G
AD  - Department of Thoracic and Cardiovascular Surgery, The Affiliated Drum Tower 
      Hospital of Nanjing University Medical School, Nanjing, Jiangsu, China.
FAU - Xu, Can
AU  - Xu C
AD  - Department of Thoracic and Cardiovascular Surgery, The Affiliated Drum Tower 
      Hospital of Nanjing University Medical School, Nanjing, Jiangsu, China.
FAU - Song, Zhizhao
AU  - Song Z
AD  - Department of Thoracic and Cardiovascular Surgery, The Affiliated Drum Tower 
      Hospital of Nanjing University Medical School, Nanjing, Jiangsu, China.
FAU - Li, Kunsheng
AU  - Li K
AD  - Department of Thoracic and Cardiovascular Surgery, The Affiliated Drum Tower 
      Hospital of Nanjing University Medical School, Nanjing, Jiangsu, China.
FAU - Zhong, Kai
AU  - Zhong K
AD  - Department of Thoracic and Cardiovascular Surgery, The Affiliated Drum Tower 
      Hospital of Nanjing University Medical School, Nanjing, Jiangsu, China.
FAU - Wang, Dongjin
AU  - Wang D
AUID- ORCID: 0000-0002-5274-8067
AD  - Department of Thoracic and Cardiovascular Surgery, The Affiliated Drum Tower 
      Hospital of Nanjing University Medical School, Nanjing, Jiangsu, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Bioengineered
JT  - Bioengineered
JID - 101581063
RN  - 0 (ATF3 protein, human)
RN  - 0 (Activating Transcription Factor 3)
RN  - 0 (Atf3 protein, mouse)
RN  - 0 (MIRN145 microRNA, human)
RN  - 0 (MIRN145a microRNA, mouse)
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Circular)
RN  - 11128-99-7 (Angiotensin II)
SB  - IM
MH  - *Activating Transcription Factor 3/genetics/metabolism
MH  - Angiotensin II
MH  - Animals
MH  - *Cardiomegaly/genetics/metabolism/pathology
MH  - Humans
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - *MicroRNAs/genetics/metabolism
MH  - Myocytes, Cardiac/cytology
MH  - *RNA, Circular/genetics/metabolism
MH  - Signal Transduction
PMC - PMC8806771
OTO - NOTNLM
OT  - ATF3
OT  - Hypertrophy
OT  - Nfix
OT  - circNfix
OT  - circRNA
OT  - miRNA
COIS- No potential conflict of interest was reported by the author(s).
EDAT- 2021/09/02 06:00
MHDA- 2021/12/24 06:00
PMCR- 2021/09/01
CRDT- 2021/09/01 12:19
PHST- 2021/09/01 12:19 [entrez]
PHST- 2021/09/02 06:00 [pubmed]
PHST- 2021/12/24 06:00 [medline]
PHST- 2021/09/01 00:00 [pmc-release]
AID - 1960462 [pii]
AID - 10.1080/21655979.2021.1960462 [doi]
PST - ppublish
SO  - Bioengineered. 2021 Dec;12(1):5373-5385. doi: 10.1080/21655979.2021.1960462.