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Cardiac Proteome Profiling in Ischemic and Dilated Cardiomyopathy Mouse Models

Danbo Lu1, Yan Xia1, Zhangwei Chen1

  • 1Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.

Frontiers in Physiology
|July 6, 2019
PubMed

Insights

This study reveals key protein changes in heart failure (HF) mouse models, highlighting altered oxidative phosphorylation and metabolism. Understanding these proteomic differences offers insights into HF

Area of Science:

  • Cardiovascular Biology
  • Proteomics
  • Molecular Medicine

Background:

  • Heart failure (HF) presents a global health challenge with significant morbidity and mortality.
  • Understanding the underlying pathophysiological mechanisms is crucial for developing effective prevention and personalized therapies for HF.

Purpose of the Study:

  • To investigate and compare the proteomic profiles of mouse models with ischemic cardiomyopathy (ICM) and dilated cardiomyopathy (DCM).
  • To identify differentially expressed proteins and pathways involved in the pathogenesis of different HF types.

Main Methods:

  • Established mouse models for ICM (myocardial infarction) and DCM (Coxsackievirus B3 infection).
  • Utilized quantitative proteomics (isobaric tags for relative and absolute quantitation, LC-MS/MS) to analyze protein expression in control and failing hearts.
  • Performed bioinformatics analyses (Gene Ontology, KEGG, Ingenuity Pathway Analysis) to interpret proteomic data.

Main Results:

  • Identified 1,638 proteins, with 286 differentially expressed between control and failing hearts.
  • Commonly modulated pathways in both ICM and DCM included oxidative phosphorylation, metabolism, and protein folding.
  • Distinct proteomic differences were observed between ICM and DCM, particularly in oxidative phosphorylation, metabolic, and AMPK signaling pathways.
  • Confirmed down-regulation of SDHB and up-regulation of UQCRQ, GLUT4, and adiponectin in specific HF models.
  • Observed decreased adenosine triphosphate (ATP) levels and differential regulation of phospho-AMPKα in ICM and DCM hearts.

Conclusions:

  • Oxidative phosphorylation, cardiac metabolism, and protein folding are critical in HF pathogenesis.
  • The distinct proteomic profiles between ICM and DCM underscore the heterogeneity of heart failure.
  • Detailed proteomic analysis provides a foundation for developing more targeted therapeutic strategies for diverse HF etiologies.

Keywords:
dilated cardiomyopathyheart failureischemic cardiomyopathymetabolismproteomics

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