AMPK and O-GlcNAcylation: interplay in cardiac pathologies and heart failure

Ettore Vanni1, Christophe Beauloye1,2, Sandrine Horman1

  • 1Pole of Cardiovascular Research, Institute of Experimental and Clinical Research (IREC), UCLouvain, Brussels, Belgium.

Essays in Biochemistry
|September 25, 2024
PubMed

Insights

Heart failure (HF) involves complex molecular changes. This review explores how AMP-activated protein kinase (AMPK) and O-GlcNAcylation impact cardiac function and metabolism in HF.

Area of Science:

  • Biochemistry
  • Cardiology
  • Molecular Biology

Background:

  • Heart failure (HF) is a significant global health issue with high morbidity and mortality.
  • Despite medical advances, understanding HF pathogenesis at the molecular level is crucial.
  • AMP-activated protein kinase (AMPK) and O-GlcNAcylation are implicated in cellular energy regulation.

Purpose of the Study:

  • To review the roles of AMPK and O-GlcNAcylation in heart failure.
  • To elucidate the interplay and dysregulation of these pathways in HF.
  • To highlight therapeutic strategies targeting AMPK and O-GlcNAcylation in HF.

Main Methods:

  • Comprehensive literature review of preclinical and clinical studies.
  • Analysis of molecular mechanisms involving AMPK and O-GlcNAcylation in cardiac function.
  • Examination of signalling pathways related to cardiac energetics, metabolism, and remodelling.

Main Results:

  • AMPK and O-GlcNAcylation are key regulators of cardiac metabolism and energetics.
  • Dysregulation of these pathways contributes to the progression of heart failure.
  • Targeting AMPK and O-GlcNAcylation shows potential for novel HF therapies.

Conclusions:

  • AMPK and O-GlcNAcylation pathways are critically involved in heart failure pathogenesis.
  • Understanding their intricate mechanisms offers new therapeutic avenues for HF.
  • Further research into these molecular targets may improve HF management.

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