Related Experiment Video
Updated: Aug 19, 2025
Isolation and Functional Analysis of Mitochondria from Cultured Cells and Mouse Tissue
Published on: March 23, 2015
Atherosclerosis: From the Disruption of Mitochondrial Membrane Potential to the Potential Interventional Strategies
Dexiang Xia1, Yanmei Chen1, Guifang Luo2
1Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, Hunan International Scientific and Technological Cooperation Base of Arteriosclerotic Disease, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.
Insights
Mitochondrial membrane potential disruption drives atherosclerosis (AS) by increasing oxidative stress, apoptosis, and NLRP3 inflammasome activation. Targeting these pathways offers potential therapeutic strategies for cardiovascular disease.
Area of Science:
- Cardiovascular Science
- Mitochondrial Biology
- Inflammation Research
Background:
- Atherosclerosis (AS) is a chronic inflammatory arterial disease and a primary cause of cardiovascular disease (CVD).
- Mitochondrial dysfunction, specifically the disruption of mitochondrial membrane potential (Δψm), is increasingly recognized as a key factor in AS pathogenesis.
- This disruption impacts cellular processes vital to AS development.
Approach:
- This review synthesizes current research on the role of Δψm disruption in AS.
- It examines the mechanisms linking Δψm alteration to oxidative stress, apoptosis, and NLRP3 inflammasome activation.
- Potential therapeutic targets within these pathways are discussed.
Key Points:
- Disruption of Δψm impairs the electron transport chain (ETC), leading to increased oxidative stress.
- Altered Δψm promotes cellular apoptosis, a hallmark of atherosclerotic plaque progression.
- Activated NLRP3 inflammasome, downstream of Δψm disruption, exacerbates arterial inflammation in AS.
Conclusions:
- Δψm disruption is a critical mediator in the development of atherosclerosis through oxidative stress, apoptosis, and NLRP3 inflammasome activation.
- Targeting these mitochondrially-driven pathways presents promising therapeutic avenues for AS intervention.
- Further research into mitochondrial function could unlock novel strategies for preventing and treating cardiovascular disease.
Abstract:
Atherosclerosis (AS) is the major factor of cardiovascular disease (CVD) and is characterized by a progressive and chronic inflammatory process in the arterial wall. Recent studies have shown that disruption of the mitochondrial membrane potential (deltapsi (m)) directly affects the electron transport chain (ETC), which in turn leads to oxidative stress, and furthermore, its alteration leads to apoptosis and activation of the NLRP3 inflammasome, thereby promoting the development of AS. Here, this review describes how deltapsi (m) contributes to the development of AS by mediating oxidative stress, apoptosis, and NLRP3 inflammasome activation, and potential AS intervention strategies by targeting oxidative stress, apoptosis, and NLRP3 inflammasome activation induced by deltapsi (m).
More Related Videos
Related Concept Videos
01:26Atherosclerosis III: Management
01:45Mitochondrial Membranes
01:30Atherosclerosis I: Introduction
01:46Electron Transport Chain: Complex I and II
ROS generation is regulated and maintained at moderate levels necessary...
01:23Atherosclerosis IV: Nursing Management
01:17Ischemic Heart Disease: Overview
Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and...