ArticleFrontiers in immunology2024
Mitochondrial dysfunction and metabolic reprogramming induce macrophage pro-inflammatory phenotype switch and atherosclerosis progression in aging.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed.
- Modulatory effects of S1QEL on OxLDL-induced metabolic alterations and inflammatory responses in human monocytes.Immunometabolism (Cobham, Surrey) · 2026Article
- Reprogramming macrophage metabolism for cardiovascular therapy: From molecular pathways to precision nanomedicine.Materials today. Bio · 2026Review
- Emerging Role of Sodium-Glucose Cotransporter-2 Inhibitors in Aortic Stenosis.JACC. Basic to translational science · 2026Review
- Mitochondrial homeostasis: the central hub governing the progression of atherosclerosis.Precision clinical medicine · 2026Review
- The Influence of Basic Therapy and New Drugs on NO-Dependent Mechanisms of Cardiac Destruction in Chronic Heart Failure.Biomedicines · 2026Review
- Aging-AssociatedJournal of the American Heart Association · 2026Article
- Article
- Integrated multi-omics profiling of plasma extracellular vesicles reveals the hsa-miR-1-3p-LRP1 axis as a potential biomarker in cervical cancer.Molecular and clinical oncology · 2026Article
- Ferroptosis in arterial atherosclerosis: mechanistic hypotheses, cell type specific vulnerabilities, translational biomarkers, and therapeutic opportunities.Frontiers in immunology · 2026Review
- Identification of core genes and transcription factors related to metabolic reprogramming in atherosclerosis: a multi-omics analysis and experimental validation approach.Frontiers in molecular biosciences · 2026Article
- Impact of exercise intervention on immune function during aging.Frontiers in immunology · 2026Review
- HYQTD Drug-containing Serum Alleviates HCurrent pharmaceutical biotechnology · 2026Article
- Mitochondrial Dysfunction Associated with mtDNA Mutation: Mitochondrial Genome Editing in Atherosclerosis Research.Current medicinal chemistry · 2026Article
- Gingerenone A attenuates diabetic vascular remodeling through AMPK/mTOR/S6K1 signaling.Frontiers in pharmacology · 2026Article
- The role of macrophages in aortic physiology and pathophysiology.Frontiers in immunology · 2026Review
- Adipose-derived mesenchymal stromal cell-microenvironment interaction network in metabolic syndrome: ADMSC injury response, adaptive regulation, and regenerative potential.Frontiers in cell and developmental biology · 2026Review
- Pathological mechanisms and research progress of multilevel intervention therapy for coronary heart disease.Frontiers in immunology · 2026Review
- Macrophage Trem2 deficiency aggravates aging-induced vascular remodeling by acting as a non-classical receptor of interleukin-13.Molecular biomedicine · 2025Article
- Cellular and molecular mechanisms underlying cardiovascular aging.Cellular & molecular biology letters · 2025Review
- Dysregulated Redox Signaling and Its Impact on Inflammatory Pathways, Mitochondrial Dysfunction, Autophagy and Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Aging increases the risk of atherosclerotic vascular disease and its complications. Macrophages are pivotal in the pathogenesis of vascular aging, driving inflammation and atherosclerosis progression. NOX4 (NADPH oxidase 4) expression increases with age, correlating with mitochondrial dysfunction, inflammation, and atherosclerosis. We hypothesized that the NOX4-dependent mitochondrial oxidative stress promotes aging-associated atherosclerosis progression by causing metabolic dysfunction and inflammatory phenotype switch in macrophages. Methods: We studied atherosclerotic lesion morphology and macrophage phenotype in young (5-month-old) and aged (16-month-old) Results: Young Discussion: Our findings suggest that increased NOX4 in aging drives macrophage mitochondrial dysfunction, glycolytic metabolic switch, and pro-inflammatory phenotype, advancing atherosclerosis. Inhibiting NOX4 or mitochondrial dysfunction could alleviate vascular inflammation and atherosclerosis, preserving plaque integrity.
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