ArticleCirculation research2014
Macrophage mitochondrial oxidative stress promotes atherosclerosis and nuclear factor-κB-mediated inflammation in macrophages.
Article in Circulation research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers.
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Who cites it
151 citing papers in PubMed, 264 citations in OpenAlex.
- Review
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- Mitochondrial cardiovascular diseases: molecular mechanisms, multi-omics exploration and therapeutic strategies.Journal of advanced research · 2026Review
- Restoring immune homeostasis in atherosclerotic plaques via inorganic violet phosphorus nano-immunotherapy.Cell reports. Medicine · 2026Article
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- Increased mROS Generation Associates With Cardiovascular Risk in BioHEART-CT PBMCs.Clinical and translational science · 2026Article
- Phytochemical Monomers Derived from Traditional Chinese Medicine May Prevent and Treat Atherosclerosis by Modulating the Macrophage Mitochondrial-Lysosomal Senescence Axis.International journal of general medicine · 2026Review
- Plaque-Targeted Delivery of Fluoride-Free MXene Nanozyme for Alleviating Atherosclerosis via Sonocatalytic Therapy.Advanced materials (Deerfield Beach, Fla.) · 2025Article
- Electrochemical detection of cardiovascular diseases and treatment platform based on microfluidic technology.Mikrochimica acta · 2025Review
- Dysregulated Redox Signaling and Its Impact on Inflammatory Pathways, Mitochondrial Dysfunction, Autophagy and Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- GDF11-secreting cell transplant efficiently ameliorates age-related pulmonary fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Pyruvate Carboxylase in Macrophages Aggravates Atherosclerosis by Regulating Metabolism Reprogramming to Promote Inflammatory Responses Through the Hypoxia-Inducible Factor-1 Signaling Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- A programmable platelet theranostic platform for adaptive multi-stage delivery and synergistic immunotherapy in atherosclerosis.Nature communications · 2025Article
- Wogonin Attenuates Atherosclerosis via KLF11-Mediated Suppression of PPARα-YAP1-Driven Glycolysis and Enhancement of ABCA1/G1-Mediated Cholesterol Efflux.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Fucosterol exerts an anti-atherosclerotic action via NF-κB and p38/Erk MAPK signaling pathways.Atherosclerosis plus · 2025Article
- Mitochondrial Dysfunction in the Development and Progression of Cardiometabolic Diseases: A Narrative Review.Journal of clinical medicine · 2025Review
91 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
rationaleMitochondrial oxidative stress (mitoOS) has been shown to correlate with the progression of human atherosclerosis. However, definitive cell type-specific causation studies in vivo are lacking, and the molecular mechanisms of potential proatherogenic effects remain to be determined.
objectiveOur aims were to assess the importance of macrophage mitoOS in atherogenesis and to explore the underlying molecular mechanisms. METHODS AND
resultsWe first validated Western diet-fed Ldlr(-/-) mice as a model of human mitoOS-atherosclerosis association by showing that non-nuclear oxidative DNA damage, a marker of mitoOS in lesional macrophages, correlates with aortic root lesion development. To investigate the importance of macrophage mitoOS, we used a genetic engineering strategy in which the OS suppressor catalase was ectopically expressed in mitochondria (mCAT) in macrophages. MitoOS in lesional macrophages was successfully suppressed in these mice, and this led to a significant reduction in aortic root lesional area. The mCAT lesions had less monocyte-derived cells, less Ly6c(hi) monocyte infiltration into lesions, and lower levels of monocyte chemotactic protein-1. The decrease in lesional monocyte chemotactic protein-1 was associated with the suppression of other markers of inflammation and with decreased phosphorylation of RelA (NF-κB p65), indicating decreased activation of the proinflammatory NF-κB pathway. Using models of mitoOS in cultured macrophages, we showed that mCAT suppressed monocyte chemotactic protein-1 expression by decreasing the activation of the IκB-kinase β-RelA NF-κB pathway.
conclusionsMitoOS in lesional macrophages amplifies atherosclerotic lesion development by promoting NF-κB-mediated entry of monocytes and other inflammatory processes. In view of the mitoOS-atherosclerosis link in human atheromata, these findings reveal a potentially new therapeutic target to prevent the progression of atherosclerosis.
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