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Molecular Mechanisms and Epigenetic Regulation in Diabetic Cardiomyopathy

Anupam Mittal1, Rajni Garg2, Ajay Bahl3

  • 1Department of Translational and Regenerative Medicine, Postgraduate Institute of Medical Education and Research, Chandigarh, India.

Frontiers in Cardiovascular Medicine
|January 3, 2022
PubMed

Insights

Type 2 diabetes contributes to cardiovascular issues like diabetic cardiomyopathy (DbCM). This review explores how epigenetic modifications, including DNA methylation and non-coding RNAs, influence DbCM development and progression.

Area of Science:

  • Cardiovascular Science
  • Metabolic Disorders
  • Epigenetics

Background:

  • Type 2 diabetes mellitus (DM) is a major lifestyle disease linked to cardiovascular diseases (CVD).
  • Diabetic cardiomyopathy (DbCM) is a cardiac complication of DM, characterized by cardiac remodeling independent of other comorbidities.
  • DbCM involves impaired cardiac metabolism, mitochondrial dysfunction, oxidative stress, inflammation, apoptosis, and autophagy.

Purpose of the Study:

  • To review the role of epigenetic modifications in the pathogenesis of diabetic cardiomyopathy (DbCM).
  • To elucidate how epigenetic mechanisms regulate molecular pathways involved in DbCM.

Main Methods:

  • Literature review focusing on epigenetic mechanisms in DbCM.
  • Analysis of studies investigating histone modifications (acetylation, methylation), DNA methylation, and non-coding RNAs in DbCM.

Main Results:

  • Epigenetic modifiers are critical in DbCM development.
  • Histone modifications, DNA methylation, and non-coding RNAs significantly impact molecular pathways underlying DbCM pathophysiology.

Conclusions:

  • Epigenetic modifications play a crucial role in the development and progression of diabetic cardiomyopathy.
  • Targeting epigenetic mechanisms offers potential therapeutic strategies for managing DbCM in diabetic patients.

Keywords:
apoptosiscardiac remodelingdiabetes mellitusdiabetic cardiomyopathyepigeneticsmitochondrial functionoxidative stress

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