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Long noncoding RNA Chast promotes cardiac remodeling.

Janika Viereck1, Regalla Kumarswamy2, Ariana Foinquinos2

  • 1Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Integriertes Forschungs- und Behandlungszentrum Transplantation (IFB-Tx), Hannover Medical School, D-30625 Hannover, Germany. Excellence Cluster REBIRTH, Hannover Medical School, D-30625 Hannover, Germany.

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Long noncoding RNAs (lncRNAs) are implicated in cardiac hypertrophy. The lncRNA Chast promotes cardiomyocyte hypertrophy by inhibiting autophagy, suggesting Chast as a therapeutic target for heart disease.

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Area of Science:

  • Cardiovascular Biology
  • Molecular Genetics
  • Noncoding RNA Research

Background:

  • Long noncoding RNAs (lncRNAs) are increasingly recognized for their roles in cardiac development.
  • However, their specific involvement in cardiac diseases like hypertrophy remains largely unexplored.
  • Understanding lncRNA dysregulation is crucial for identifying novel therapeutic targets in heart conditions.

Purpose of the Study:

  • To investigate the role of lncRNAs in pressure overload-induced cardiac hypertrophy.
  • To identify and characterize novel lncRNA candidates involved in cardiomyocyte hypertrophy.
  • To elucidate the molecular mechanisms by which identified lncRNAs regulate cardiac remodeling.

Main Methods:

  • Global lncRNA expression profiling in mouse models of cardiac hypertrophy.
  • Identification and validation of candidate lncRNAs using stringent selection criteria.
  • In vitro and in vivo experiments involving lncRNA overexpression and silencing (GapmeR).
  • Cell fractionation, human patient sample analysis, and mechanistic studies involving protein interactions.

Main Results:

  • Several lncRNA transcripts were found to be deregulated during pressure overload-induced cardiac hypertrophy.
  • The cardiac hypertrophy-associated transcript (Chast) was identified as a key lncRNA influencing cardiomyocyte hypertrophy.
  • Chast is upregulated in cardiomyocytes in vivo and in human hypertrophic hearts, and its overexpression induces hypertrophy.
  • Silencing Chast prevented and attenuated cardiac remodeling in mice without apparent toxicity.
  • Chast negatively regulates Pleckstrin homology domain-containing protein family M member 1, inhibiting cardiomyocyte autophagy and promoting hypertrophy.

Conclusions:

  • Chast is a critical lncRNA that drives cardiomyocyte hypertrophy and pathological cardiac remodeling.
  • Chast represents a potential therapeutic target for preventing or treating cardiac hypertrophy and related heart diseases.
  • This study underscores the significant role of lncRNAs in the pathogenesis of cardiovascular diseases.