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An Approach to Study Shape-Dependent Transcriptomics at a Single Cell Level
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Deciphering transcriptional dynamics of cardiac hypertrophy and failure in a chamber-specific manner

Dan Zhang1, Jianming Liu1, Haiying Xiao2

  • 1Key Laboratory of Medical Electrophysiology, Ministry of Education and Medical Electrophysiological Key Laboratory of Sichuan Province, and Collaborative Innovation Center for Prevention of Cardiovascular Diseases, Institute of Cardiovascular Research, Southwest Medical University, Luzhou, China.

Biomolecules & Biomedicine
|June 19, 2023
PubMed

Insights

This study identified key genes and pathways in pathological cardiac hypertrophy (CH) and heart failure (HF) after pressure overload. It highlights shared molecular mechanisms and potential biomarkers for these dynamic cardiac remodeling processes.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Genomics

Background:

  • Pathological cardiac hypertrophy (CH) and subsequent heart failure (HF) result from pressure overload, involving complex cardiac remodeling.
  • The precise biological mechanisms underlying the transition from CH to HF remain incompletely understood.
  • Identifying key genes and pathways is crucial for understanding and potentially treating these conditions.

Purpose of the Study:

  • To identify differentially expressed genes (DEGs) associated with CH and HF in different heart chambers following aortic arch constriction (TAC).
  • To investigate shared and distinct molecular mechanisms during the dynamic transition from CH to HF.
  • To determine potential gene biomarkers and essential hub genes involved in cardiac remodeling.

Main Methods:

  • Utilized a mouse model of pressure overload (aortic arch constriction).
  • Performed whole cardiac transcriptome analysis to identify DEGs in the left atrium (LA), left ventricle (LV), and right ventricle (RV) at 4 (CH) and 6 (HF) weeks post-TAC.
  • Conducted functional enrichment analysis and identified hub genes.

Main Results:

  • Identified significant numbers of DEGs for CH and HF across all three heart chambers.
  • Discovered shared DEGs (e.g., elastin, HBB-BS) across chambers and specific DEGs common to LA/LV and LV/RV in both CH and HF.
  • Highlighted the roles of extracellular matrix and sarcolemma, and identified LOX, FGF, and NDUF families as key hub genes in the CH to HF transition.

Conclusions:

  • The study provides a comprehensive transcriptomic landscape of cardiac remodeling during the progression from CH to HF.
  • Identified DEGs and hub genes offer potential biomarkers for diagnosing and understanding the dynamic changes in cardiac function.
  • Findings elucidate critical molecular pathways, including extracellular matrix and sarcolemma involvement, essential for cardiac remodeling.

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