Related Experiment Video

Updated: Sep 20, 2025

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
08:43

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation

Published on: May 31, 2016

19.7K

Phosphoglycerate Mutase 5 Is Important Mediator for Instigating Arterial Lipid Accumulation and Aggravating

Qian Zhang1, Peng Zheng1, Yang Pan2

  • 1Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.

JACC. Basic to Translational Science
|May 28, 2025
PubMed

Insights

Phosphoglycerate mutase 5 (PGAM5) is elevated in atherosclerosis, worsening lesions. Inhibiting PGAM5 in macrophages reduces inflammation and cell migration, suggesting PGAM5 as a therapeutic target for atherosclerosis.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Inflammation Research

Background:

  • The receptor-interacting protein kinase-3 (RIPK3)-phosphoglycerate mutase 5 (PGAM5) pathway is implicated in various diseases.
  • The specific role of the RIPK3-PGAM5 pathway in the pathogenesis of atherosclerotic lesions is not well understood.

Purpose of the Study:

  • To investigate the role and mechanism of the RIPK3-PGAM5 signaling pathway in atherosclerosis.
  • To determine if PGAM5 could be a potential therapeutic target for atherosclerosis.

Main Methods:

  • Analysis of phosphorylated RIPK3 and PGAM5 expression in human and mouse atherosclerosis lesions.
  • In vivo and in vitro models to study the effects of PGAM5 overexpression.
  • Macrophage-specific PGAM5 knockdown to assess its impact on gene expression and cellular functions.
  • Evaluation of inflammatory factor release and cell migration in endothelial and smooth muscle cells.

Main Results:

  • Phosphorylated RIPK3 and PGAM5 levels are significantly increased in macrophages within atherosclerotic lesions.
  • PGAM5 overexpression exacerbates atherosclerotic lesion development in experimental models.
  • Knockdown of PGAM5 in macrophages leads to increased angiopoietin-like 3 (ANGPTL3) expression.
  • PGAM5 inhibition reduces inflammatory factor release and inhibits endothelial and smooth muscle cell migration.

Conclusions:

  • PGAM5 plays a critical role in mediating atherosclerosis.
  • Targeting PGAM5 in macrophages may offer a novel therapeutic strategy for treating atherosclerosis.
Keywords:
angiopoietin-like protein 3atherosclerosismacrophagesphosphoglycerate mutase 5receptor-interacting protein kinase-3

More Related Videos

Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro09:41

Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro

Published on: March 17, 2023

3.1K
Author Spotlight: Exploring the Relationship Between Lipotoxicity and HFpEF03:42

Author Spotlight: Exploring the Relationship Between Lipotoxicity and HFpEF

Published on: March 29, 2024

1.7K

Related Concept Videos

Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
97
Peripheral Artery Disease I: Introduction01:30

Peripheral Artery Disease I: Introduction

Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs, particularly the arteries supplying the thighs and calves. In rare cases, it may involve other arteries, including those in the arms.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty...
37
Overview of Lipid Metabolism01:24

Overview of Lipid Metabolism

Lipid metabolism is a crucial process in the human body that involves the synthesis and degradation of lipids. This process is essential for energy production, cell membrane formation, and hormone production, among other functions.
Lipolysis: The Breakdown of Lipids:
Lipolysis is the process of breaking down lipids, particularly triglycerides, into glycerol and fatty acids. This process typically occurs in the adipose tissue and is triggered by various hormones, including glucagon and...
2.6K
Inflammation01:38

Inflammation

Overview
55.5K
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
44
Atherosclerosis III: Management01:26

Atherosclerosis III: Management

Management of atherosclerosis involves an integrated strategy encompassing pharmacological treatment, surgical interventions, lifestyle changes, and nutrition therapy to address the multifactorial nature of the disease.Pharmacological TherapyA cornerstone of atherosclerosis management is the use of pharmacological agents. Statins, such as atorvastatin, are pivotal in inhibiting HMG-CoA reductase, an enzyme that catalyzes an initial step in cholesterol synthesis in the liver. This reduction in...
42