Related Experiment Video
Updated: Sep 8, 2025
08:05
Optimization of Transesophageal Atrial Pacing to Assess Atrial Fibrillation Susceptibility in Mice
Published on: June 29, 2022
2.9K
PFKM-Driven Lactate Overproduction Promotes Atrial Fibrillation via Triggering Cardiac Fibroblasts Histone
Ning Fang1, Ning Zhang1, Xiaohui Jiang1
1Department of Cardiology, The First Affiliated Hospital, Harbin Medical University, Harbin, 150001, China.
Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|June 26, 2025
Summary
Enhanced glycolysis promotes atrial fibrillation (AF) by increasing lactate, leading to atrial fibrosis through histone lactylation. Targeting this metabolic-epigenetic axis may offer new AF therapies.
Area of Science:
- Biochemistry
- Epigenetics
- Cardiology
Background:
- Atrial fibrillation (AF) is linked to increased glycolysis and lactate.
- The role of glycolysis and histone lactylation in AF pathogenesis is unclear.
Purpose of the Study:
- To investigate if glycolysis promotes AF development.
- To explore the role of histone lactylation in AF pathogenesis.
- To elucidate the metabolic-epigenetic mechanisms underlying AF.
Main Methods:
- Established spontaneous atrial fibrillation (AF) mouse models.
- Utilized glycolysis inhibitor (2-deoxyglucose) and PFKM gene expression.
- Analyzed cardiac fibroblast activation and histone lactylation (H3K18 lactylation).
Main Results:
- Enhanced glycolysis promotes AF development and atrial fibrosis in mice.
- Lactate stimulates cardiac fibroblast activation and H3K18 lactylation.
- P300-mediated H3K18 lactylation up-regulates TGF-β1, causing fibrosis.
Conclusions:
- Glycolysis promotes AF through a metabolic-epigenetic axis involving histone lactylation.
- Histone lactylation of H3K18 in fibroblasts contributes to AF-associated fibrosis.
- Targeting the metabolic-epigenetic pathway presents potential therapeutic strategies for AF.
More Related Videos
Related Concept Videos
01:24Muscle Recovery and Fatigue
2.5K
Muscle fatigue refers to the decline in a muscle's ability to maintain the force of contraction after prolonged activity. It primarily stems from changes within muscle fibers. Even before experiencing muscle fatigue, one may feel tired and have the urge to stop the activity. This response, known as central fatigue, occurs due to changes in the central nervous system, namely the brain and spinal cord. While there is no single mechanism that induces fatigue, it may serve as a protective...
2.5K
01:25cAMP-dependent Protein Kinase Pathways
6.6K
Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
6.6K
01:29Heart Failure II: Pathophysiology
33
Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
33
01:09Introduction to Fibroblasts
3.2K
Rudolph Virchow discovered spindle-shaped cells called fibroblasts in 1858. Inactive fibroblasts, called fibrocytes, become activated by various stimuli, such as growth factors and inflammatory cytokines. Activated fibroblasts play a crucial role in wound healing, inflammation, formation of new blood vessels, and cancer progression. Uncontrolled activation of fibroblasts results in fibrosis, the excess deposition of fibrous tissue, which can lead to scarring and affect normal organs. This...
3.2K