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Nuclear receptor corepressor 1 represses cardiac hypertrophy

Chao Li1,2,3, Xue-Nan Sun1,2,4, Bo-Yan Chen1,2

  • 1Laboratory of Oral Microbiota and Systemic Diseases, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

EMBO Molecular Medicine
|September 19, 2019
PubMed

Insights

Nuclear receptor corepressor 1 (NCoR1) normally prevents cardiac hypertrophy. Its absence worsens heart enlargement and dysfunction, suggesting NCoR1 is a therapeutic target for heart conditions.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Epigenetics

Background:

  • The role of nuclear receptor corepressor 1 (NCoR1) in heart cells (cardiomyocytes) is not well understood.
  • Its involvement in both normal heart function and disease states like cardiac hypertrophy remains unclear.

Purpose of the Study:

  • To investigate the function of NCoR1 in cardiomyocytes.
  • To determine the physiological and pathological implications of NCoR1 in the context of cardiac hypertrophy.

Main Methods:

  • Generated cardiomyocyte-specific NCoR1 knockout (CMNKO) mice for in vivo studies.
  • Utilized cell culture models to study NCoR1's effects on phenylephrine-induced cardiomyocyte hypertrophy.
  • Performed mechanistic studies involving protein-protein interactions and gene expression analysis.

Main Results:

  • CMNKO mice exhibited baseline cardiac hypertrophy and exacerbated dysfunction under pressure overload.
  • NCoR1 knockdown worsened hypertrophy, while overexpression mitigated it.
  • NCoR1 was found to interact with MEF2a and HDACs to suppress hypertrophy-related genes.

Conclusions:

  • NCoR1 plays a crucial role in repressing cardiac hypertrophy by cooperating with MEF2 and HDACs.
  • Targeting NCoR1 and the MEF2/HDACs complex presents a potential therapeutic strategy for pathological cardiac hypertrophy.
Keywords:
MEF2acardiac hypertrophyclass IIa HDACsnuclear receptor corepressor 1

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