Related Experiment Video
Updated: Jun 12, 2025

Measurement of Insulin- and Contraction-Stimulated Glucose Uptake in Isolated and Incubated Mature Skeletal Muscle from Mice
Published on: May 16, 2021
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.
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.
Abstract:
Heart failure (HF) represents a multifaceted clinical syndrome characterized by the heart's inability to pump blood efficiently to meet the body's metabolic demands. Despite advances in medical management, HF remains a major cause of morbidity and mortality worldwide. In recent years, considerable attention has been directed toward understanding the molecular mechanisms underlying HF pathogenesis, with a particular focus on the role of AMP-activated protein kinase (AMPK) and protein O-GlcNAcylation. This review comprehensively examines the current understanding of AMPK and O-GlcNAcylation signalling pathways in HF, emphasizing their interplay and dysregulation. We delve into the intricate molecular mechanisms by which AMPK and O-GlcNAcylation contribute to cardiac energetics, metabolism, and remodelling, highlighting recent preclinical and clinical studies that have explored novel therapeutic interventions targeting these pathways.
More Related Videos
Related Concept Videos
Pathophysiology of Heart Failure
cAMP-dependent Protein Kinase Pathways
Transducer Mechanism: Enzyme-Linked Receptors
Major types that are helpful drug targets include:
Pathophysiology of Cardiac Performance
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Heart Failure Drugs: Inotropic Agents

