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Signal transducer and transcriptional activation 1 protects against pressure overload-induced cardiac hypertrophy

Changlin Zhen1, Hongxia Liu1, Li Gao1

  • 1State Key Laboratory of Natural Medicines, Department of Pharmacology, China Pharmaceutical University, Nanjing, China.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|December 30, 2020
PubMed

Insights

Signal transducers and transcriptional activation 1 (Stat1) protects against cardiac hypertrophy. Stat1 inhibits fibrosis and enhances mitochondrial function via the Ucp2/P-Drp1 pathway, preserving cardiomyocyte function.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Cellular Signaling

Background:

  • Signal transducers and transcriptional activation (STATs) proteins regulate diverse cellular processes.
  • The role of Stat1 in pathological cardiac hypertrophy remains largely uncharacterized.
  • Cardiac hypertrophy involves complex molecular and cellular changes impacting heart function.

Purpose of the Study:

  • To elucidate the function of Stat1 in pathological cardiac hypertrophy.
  • To investigate the protective mechanisms of Stat1 in the heart.
  • To identify molecular pathways modulated by Stat1 in cardiac hypertrophy.

Main Methods:

  • Utilized H9C2 cardiomyocytes and cardiomyocyte-specific Stat1/IfngR knockout mice.
  • Induced cardiac hypertrophy using transverse aortic constriction (TAC) in mice.
  • Assessed cardiac hypertrophy via echocardiography, histopathology, and molecular analyses.

Main Results:

  • Stat1 deficiency exacerbated TAC-induced cardiac hypertrophy and fibrosis.
  • Stat1 downregulated hypertrophy and fibrosis marker genes.
  • Stat1 promoted mitochondrial fission via the Ucp2/P-Drp1 pathway, enhancing mitochondrial function and ATP production.

Conclusions:

  • Stat1 exhibits a protective role against cardiac hypertrophy.
  • Stat1 inhibits cardiac hypertrophy by suppressing fibrotic and hypertrophic gene expression.
  • Stat1 enhances cardiomyocyte function and ATP production through the Ucp2/P-Drp1 pathway, mitigating cardiac hypertrophy.

Keywords:
Drp1Stat1UCP2heart function

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