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CMTM3 deficiency induces cardiac hypertrophy by regulating MAPK/ERK signaling

Jingjing Ye1, Saifang Yan2, Ruxia Liu3

  • 1Trauma Medicine Center, Peking University People's Hospital, Key Laboratory of Trauma and Neural Regeneration (Peking University), Ministry of Education, National Center for Trauma Medicine, Beijing, 100044, PR China.

Biochemical and Biophysical Research Communications
|May 25, 2023
PubMed

Insights

CMTM3 deficiency worsens cardiac hypertrophy, while its increased expression inhibits it by suppressing MAPK signaling. This suggests CMTM3 acts as a protective factor against heart enlargement and dysfunction.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Cellular Signaling

Background:

  • Cardiac hypertrophy is a compensatory heart response that can lead to heart failure.
  • Understanding factors that regulate cardiac hypertrophy is crucial for preventing adverse cardiac events.
  • The role of the CMTM3 protein in cardiac function was previously unknown.

Purpose of the Study:

  • To investigate the role and mechanism of CMTM3 in cardiac hypertrophy.
  • To determine if CMTM3 deficiency affects cardiac hypertrophy development.
  • To explore the potential of CMTM3 as a therapeutic target for cardiac hypertrophy.

Main Methods:

  • Generated Cmtm3 knockout mouse models for loss-of-function studies.
  • Utilized Angiotensin II infusion and phenylephrine stimulation to induce cardiac hypertrophy in vivo and in vitro.
  • Employed RNA sequencing and Western blotting to analyze molecular signaling pathways, including MAPK/ERK.

Main Results:

  • CMTM3 deficiency exacerbated cardiac hypertrophy and dysfunction in mice.
  • CMTM3 expression was upregulated in hypertrophic hearts and cardiomyocytes.
  • Overexpression of CMTM3 inhibited phenylephrine-induced cardiomyocyte hypertrophy and reduced MAPK/ERK pathway activation.

Conclusions:

  • CMTM3 deficiency promotes cardiac hypertrophy and worsens cardiac dysfunction.
  • Increased CMTM3 expression during hypertrophy acts to inhibit further cardiomyocyte growth.
  • CMTM3 functions as a negative regulator of cardiac hypertrophy by modulating MAPK signaling.
Abstract

Keywords:
CMTM3Cardiac hypertrophyMAPK/ERK signaling

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