Related Experiment Video

Updated: Jul 25, 2025

Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model
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Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model

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Cardiac proteomic profiling suggests that hypertrophic and dilated cardiomyopathy share a common pathogenetic pathway

Wenjuan Yang1, Yu Zhu1,2, Fuqin Tang1

  • 1Department of Cardiovascular Surgery, The Second Affiliated Hospital of Army Medical University, Chongqing, China.

European Journal of Clinical Investigation
|June 29, 2023
PubMed

Insights

Hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) share molecular pathways, particularly involving calcium signaling. Targeting these calcium-related processes and key proteins offers promising therapeutic strategies beyond genetic research for both heart conditions.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Proteomics

Background:

  • Hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) are distinct heart diseases with overlapping genetic and clinical features.
  • Previous research has primarily focused on genetic mutations, necessitating exploration of underlying molecular mechanisms.
  • Identifying shared pathogenic pathways is crucial for developing effective therapeutic targets for both HCM and DCM.

Purpose of the Study:

  • To identify key molecular mechanisms common to both HCM and DCM.
  • To explore potential therapeutic targets by analyzing differentially expressed proteins (DEPs).
  • To compare molecular differences and similarities between HCM and DCM.

Main Methods:

  • Proteomic analysis using liquid chromatography-tandem mass spectrometry on myocardial tissue from HCM, DCM, and control groups.
  • Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses to identify DEPs.
  • Western blotting to validate the expression levels of selected proteins.

Main Results:

  • Significant differences in protein expression were observed between control, HCM, and DCM groups.
  • Proteins related to contraction and actin binding were commonly affected in HCM and DCM.
  • The calcium signaling pathway emerged as a significantly altered pathway when comparing HCM and DCM, with upregulation of calcium regulation-related proteins like FKBP1A.

Conclusions:

  • HCM and DCM share common pathogenetic pathways, with calcium ion regulation being a critical factor.
  • Interfering with key calcium-related pathways or regulating linchpin protein expression may be more effective therapeutic strategies than solely focusing on genetic research for HCM and DCM.
  • This study highlights novel molecular targets for managing these complex cardiomyopathies.
Abstract

Keywords:
FKBP1Acalcium-related pathwaydilated cardiomyopathyhypertrophic cardiomyopathyproteomics

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