ArticleCirculation research2019
Mitochondrial Metabolic Reprogramming by CD36 Signaling Drives Macrophage Inflammatory Responses.
Article in Circulation research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers.
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Who cites it
161 citing papers in PubMed, 240 citations in OpenAlex.
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- Post-Traumatic Stress Disorder and Atherosclerosis: Co-Phenomena, or Cause-and-Effect?Current atherosclerosis reports · 2026Review
- Article
- Macrophage PIM1 Drives Atherosclerosis by Enhancing Foam Cell Formation Via CD36.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- CD36-mediated lipid-accumulation in reactive microglia contributes to retinal degeneration via the NLRP3-IL-1β pathway in mice.Nature communications · 2026Article
- AntagomiR-155 hitchhiking on biomimetic yeast microcapsules alleviate atherosclerosis by inhibiting M1-like macrophages.Materials today. Bio · 2026Article
- Reprogramming macrophage metabolism for cardiovascular therapy: From molecular pathways to precision nanomedicine.Materials today. Bio · 2026Review
- Differential transcriptomic and metabolomic landscape between human hearts donated after cardiac vs brain death.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2026Article
- CD36: bridging metabolism, inflammation, and reproduction.npj metabolic health and disease · 2026Review
- A Multilevel Redox-Based Prognostic Model for Asthma Severity: From Genotype to Serum Biomarkers.Biomedicines · 2026Review
- Buwang Formula Regulates Microglial Metabolic Reprogramming and Modulates the mTOR/HIF-1α Pathway to Reduce Neuroinflammation in Diabetic Mice.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Metabolic Perspective on Atherosclerosis: Macrophage Reprogramming and Novel Therapeutic Targets.Journal of the American Heart Association · 2026Review
- Cluster of Differentiation 36-Mediated Inflammation and Lipid Metabolism in Cardiovascular Diseases: From Mechanisms to Novel Therapies.Antioxidants (Basel, Switzerland) · 2026Review
- Sex Differences in Mitochondrial Function: Endocrine Regulation, Immunometabolic Signaling, and Implications for Health and Disease.International journal of molecular sciences · 2026Review
- Narcissoside attenuates atherosclerosis by suppressing CD36-mediated foam cell formation via upregulation of NR4A1.Chinese medicine · 2026Article
- A D-dimer and ADAMTS8 based multi-marker score for the diagnosis of acute aortic dissection.Scientific reports · 2026Article
- Metabolic reprogramming in aortic diseases: insights from metabolomics and therapeutic opportunities.Medical review (2021) · 2026Review
- Monocytes Defined by Platelet Interactions and Oxidative Stress Signaling Underlie HIV-Associated Atherosclerosis.Journal of the American Heart Association · 2026Article
- Ripk1-dependent PANoptosis promotes EndMT and aggravates hypoglycemia-related cardiac fibrosis in diabetes.Journal of translational medicine · 2026Article
101 more citing papers are in PubMed but not listed here.
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Authors and funding
21 authors at 2 institutions in 1 country.
Funding
Abstract
rationaleA hallmark of chronic inflammatory disorders is persistence of proinflammatory macrophages in diseased tissues. In atherosclerosis, this is associated with dyslipidemia and oxidative stress, but mechanisms linking these phenomena to macrophage activation remain incompletely understood.
objectiveTo investigate mechanisms linking dyslipidemia, oxidative stress, and macrophage activation through modulation of immunometabolism and to explore therapeutic potential targeting specific metabolic pathways. METHODS AND
resultsUsing a combination of biochemical, immunologic, and ex vivo cell metabolic studies, we report that CD36 mediates a mitochondrial metabolic switch from oxidative phosphorylation to superoxide production in response to its ligand, oxidized LDL (low-density lipoprotein). Mitochondrial-specific inhibition of superoxide inhibited oxidized LDL-induced NF-κB (nuclear factor-κB) activation and inflammatory cytokine generation. RNA sequencing, flow cytometry, 3H-labeled palmitic acid uptake, lipidomic analysis, confocal and electron microscopy imaging, and functional energetics revealed that oxidized LDL upregulated effectors of long-chain fatty acid uptake and mitochondrial import, while downregulating fatty acid oxidation and inhibiting ATP5A (ATP synthase F1 subunit alpha)-an electron transport chain component. The combined effect is long-chain fatty acid accumulation, alteration of mitochondrial structure and function, repurposing of the electron transport chain to superoxide production, and NF-κB activation.
conclusionsThese findings reveal that oxidized LDL/CD36 signaling in macrophages links dysregulated fatty acid metabolism to oxidative stress from the mitochondria, which drives chronic inflammation. Thus, targeting to CD36 and its downstream effectors may serve as potential new strategies against chronic inflammatory diseases such as atherosclerosis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.