Search research articles

Search research articles

Related Experiment Videos

Mitochondrial dysfunction in atherosclerosis.

Nageswara R Madamanchi¹, Marschall S Runge

¹Carolina Cardiovascular Biology Center, Department of Medicine, University of North Carolina, Chapel Hill, NC 27599-7005, USA.

Circulation Research

|March 3, 2007

Summary

This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Correction: Oxidative Stress, NADPH Oxidases, and Arteries.

Hamostaseologie·2026

Same author

Corrigendum to 'Obesity and natriuretic peptides, BNP and NT-proBNP: Mechanisms and diagnostic implications for heart failure' [Int J Cardiol. 2014, 176(3):611-7].

International journal of cardiology·2026

Same author

Corrigendum to 'NADPH oxidase 4 regulates vascular inflammation in aging and atherosclerosis' [Journal of Molecular and Cellular Cardiology 102 (2017) 10-21].

Journal of molecular and cellular cardiology·2026

Same author

Aging-Associated <i>Nox4</i>-Mediated Mitochondrial Reactive Oxygen Species and DNA Damage Promote Vascular Cell Reprogramming and Aortic Remodeling in Abdominal Aneurysms.

Journal of the American Heart Association·2026

Same author

Corrigendum to: "NOXA1-dependent NADPH oxidase regulates redox signaling and phenotype of vascular smooth muscle cell during atherogenesis" [Red. Biol. 71 (2019) 101063].

Redox biology·2026

Same author

Mitochondrial NOX4 drives atrial fibrillation via redox-dependent structural remodeling and fibrosis.

Free radical biology & medicine·2025

Same journal

Editors and Editorial Board.

Circulation research·2026

Same journal

Cannabis Is Associated With Potentially Proatherogenic Inflammation in Youth.

Circulation research·2026

Same journal

WTAP Deficiency Promotes Podocyte PANoptosis and FSGS via SPP1 Signaling.

Circulation research·2026

Same journal

B1a Cell-IgM Axis Protects Against Hypertension by Blunting IFNγ+CD4+T Cells.

Circulation research·2026

Same journal

SBK2 Links Cardiac Stress Signaling to Mitochondrial Proteostasis.

Circulation research·2026

Same journal

Myeloid Piezo1 as a Brake on Efferocytosis and Cardiac Repair in the Infarcted Heart.

Circulation research·2026

See all related articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Mitochondrial dysfunction, driven by oxidative stress, contributes to atherosclerosis and heart disease. This dysfunction impairs vascular cells, leading to plaque rupture and serious cardiovascular events.

Area of Science:

Biochemistry
Cardiovascular Science
Cell Biology

Background:

Mitochondrial dysfunction, characterized by increased reactive oxygen species (ROS) and DNA damage, is linked to atherosclerosis and cardiomyopathy.
Factors like hypercholesterolemia, hyperglycemia, and aging exacerbate mitochondrial dysfunction, promoting cardiovascular disease.
Oxidative stress from mitochondria contributes to beta-cell destruction, LDL oxidation, and endothelial dysfunction, all key in atherosclerosis development.

Purpose of the Study:

To review the link between mitochondrial dysfunction and clinical manifestations of atherosclerosis.
To connect findings from cell and animal models of oxidative stress to human cardiovascular syndromes.

Main Methods:

Literature review focusing on studies of reactive oxygen species generation and modulation.

Related Experiment Videos

Analysis of research linking mitochondrial dysfunction to atherosclerosis precursors and vascular cell behavior.

Main Results:

Mitochondrial dysfunction promotes atherosclerosis through ROS overproduction, LDL oxidation, and endothelial damage.
Impaired mitochondrial integrity leads to vascular cell apoptosis, plaque rupture, and subsequent cardiovascular events like myocardial infarction and stroke.
Aging and metabolic disorders significantly induce mitochondrial dysfunction, predisposing individuals to vascular diseases.

Conclusions:

Mitochondrial dysfunction is a critical factor in the pathogenesis of atherosclerosis and its complications.
Understanding the role of mitochondria in oxidative stress is crucial for developing strategies to prevent and treat cardiovascular diseases.
Targeting mitochondrial pathways may offer novel therapeutic approaches for atherosclerosis and related conditions.