ArticleArteriosclerosis, thrombosis, and vascular biology2009
Thiol oxidative stress induced by metabolic disorders amplifies macrophage chemotactic responses and accelerates atherogenesis and kidney injury in LDL receptor-deficient mice.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 64 citations in OpenAlex.
- Myeloid monoamine oxidase A protects against glucose intolerance, insulin resistance and weight gain in high-fat diet-fed mice by preventing the hyperactivation of macrophages.The Journal of nutritional biochemistry · 2026Article
- Myeloid GPSM1 regulates atherosclerosis progression by governing monocyte and macrophage activation and chemotaxis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Role of sex as a biological variable in neonatal alveolar macrophages.Redox biology · 2024Article
- Crosstalk between Oxidative Stress and Inflammation Caused by Noise and Air Pollution-Implications for Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2024Review
- Macrophage-restricted overexpression of glutaredoxin 1 protects against atherosclerosis by preventing nutrient stress-induced macrophage dysfunction and reprogramming.Atherosclerosis · 2023Article
- Glutaredoxin 1 controls monocyte reprogramming during nutrient stress and protects mice against obesity and atherosclerosis in a sex-specific manner.Nature communications · 2022Article
- Regulation of Vascular Function and Inflammation via Cross Talk of Reactive Oxygen and Nitrogen Species from Mitochondria or NADPH Oxidase-Implications for Diabetes Progression.International journal of molecular sciences · 2020Review
- Phagocytosis by macrophages depends on histamine H2 receptor signaling and scavenger receptor 1.MicrobiologyOpen · 2019Article
- Distinct Redox Signalling following Macrophage Activation Influences Profibrotic Activity.Journal of immunology research · 2019Article
- Vascular Inflammation and Oxidative Stress: Major Triggers for Cardiovascular Disease.Oxidative medicine and cellular longevity · 2019Review
- Redox-Sensitive Innate Immune Pathways During Macrophage Activation in Type 1 Diabetes.Antioxidants & redox signaling · 2018Review
- Dietary 23-hydroxy ursolic acid protects against atherosclerosis and obesity by preventing dyslipidemia-induced monocyte priming and dysfunction.Atherosclerosis · 2018Article
- The Pathogenesis of Atherosclerosis Based on Human Signaling Networks and Stem Cell Expression Data.International journal of biological sciences · 2018Article
- Mitogen-activated protein kinase phosphatase 1 (MKP-1) in macrophage biology and cardiovascular disease. A redox-regulated master controller of monocyte function and macrophage phenotype.Free radical biology & medicine · 2017Review
- Dyslipidemic Diet-Induced Monocyte "Priming" and Dysfunction in Non-Human Primates Is Triggered by Elevated Plasma Cholesterol and Accompanied by Altered Histone Acetylation.Frontiers in immunology · 2017Article
- Protein S-Glutathionylation Mediates Macrophage Responses to Metabolic Cues from the Extracellular Environment.Antioxidants & redox signaling · 2016Article
- Protein Thiol Redox Signaling in Monocytes and Macrophages.Antioxidants & redox signaling · 2016Review
- Macrophage TGF-International journal of clinical medicine · 2016Article
- Inhibition of Glutathione Production Induces Macrophage CD36 Expression and Enhances Cellular-oxidized Low Density Lipoprotein (oxLDL) Uptake.The Journal of biological chemistry · 2015Article
- Oxidative stress, redox regulation and diseases of cellular differentiation.Biochimica et biophysica acta · 2015Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundStrengthening the macrophage glutathione redox buffer reduces macrophage content and decreases the severity of atherosclerotic lesions in LDL receptor-deficient (LDLR(-/-)) mice, but the underlying mechanisms were not clear. This study examined the effect of metabolic stress on the thiol redox state, chemotactic activity in vivo, and the recruitment of macrophages into atherosclerotic lesions and kidneys of LDL-R(-/-) mice in response to mild, moderate, and severe metabolic stress. METHODS AND
resultsReduced glutathione (GSH) and glutathione disulfide (GSSG) levels in peritoneal macrophages isolated from mildly, moderately, and severe metabolically-stressed LDL-R(-/-) mice were measured by HPLC, and the glutathione reduction potential (E(h)) was calculated. Macrophage E(h) correlated with the macrophage content in both atherosclerotic (r(2)=0.346, P=0.004) and renal lesions (r(2)=0.480, P=0.001) in these mice as well as the extent of both atherosclerosis (r(2)=0.414, P=0.001) and kidney injury (r(2)=0.480, P=0.001). Compared to LDL-R(-/-) mice exposed to mild metabolic stress, macrophage recruitment into MCP-1-loaded Matrigel plugs injected into LDL-R(-/-) mice increased 2.6-fold in moderately metabolically-stressed mice and 9.8-fold in severely metabolically-stressed mice. The macrophage E(h) was a strong predictor of macrophage chemotaxis (r(2)=0.554, P<0.001).
conclusionsThiol oxidative stress enhances macrophage recruitment into vascular and renal lesions by increasing the responsiveness of macrophages to chemoattractants. This novel mechanism contributes at least in part to accelerated atherosclerosis and kidney injury associated with dyslipidemia and diabetes in mice.
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