ArticleScientific reports2020
Effects of inflammatory and anti-inflammatory environments on the macrophage mitochondrial function.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
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- Association Between Inflammatory Dietary Pattern and Cardiovascular-Kidney-Metabolic Syndrome: A Population-Based Study.Current medical science · 2025Article
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- Dysregulated cellular metabolism drives atherosclerotic plaque progression: a multi-cellular perspective.Frontiers in cardiovascular medicine · 2025Review
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- Comparative Evaluation of the Chemical Components and Anti-Inflammatory Potential of Yellow- and Blue-FloweredMetabolites · 2024Article
- Acute neuroinflammation promotes a metabolic shift that alters extracellular vesicle cargo in the mouse brain cortex.Journal of extracellular biology · 2024Article
- Actives from the Micro-Immunotherapy Medicine 2LMIREGJournal of inflammation research · 2024Article
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- Metabolic profile of mesenchymal stromal cells and macrophages in the presence of polyethylene particles in a 3D model.Stem cell research & therapy · 2023Article
- Early effects of LPS-induced neuroinflammation on the rat hippocampal glycolytic pathway.Journal of neuroinflammation · 2022Article
- Targeting immunometabolism by active ingredients derived from traditional Chinese medicines for treatment of rheumatoid arthritis.Chinese herbal medicines · 2021Review
- α-Mangostin Alleviated HIF-1α-Mediated Angiogenesis in Rats With Adjuvant-Induced Arthritis by Suppressing Aerobic Glycolysis.Frontiers in pharmacology · 2021Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial response to inflammation is crucial in the metabolic adaptation to infection. This study aimed to explore the mitochondrial response under inflammatory and anti-inflammatory environments, with a focus on the tricarboxylic acid (TCA) cycle. Expression levels of key TCA cycle enzymes and the autophagy-related protein light chain 3b (LC3b) were determined in raw 264.7 cells treated with lipopolysaccharide (LPS) and metformin (Met). Additionally, reactive oxygen species (ROS) levels and mitochondrial membrane potential were assessed using flow cytometry. Moreover, 8-week-old C57BL/6J mice were intraperitoneally injected with LPS and Met to assess the mitochondrial response in vivo. Upon LPS stimulation, the expression of key TCA enzymes, including citrate synthase, α-ketoglutarate dehydrogenase, and isocitrate dehydrogenase 2, and the mitochondrial membrane potential decreased, whereas the levels of LC3b and ROS increased. However, treatment with Met inhibited the reduction of LPS-induced enzyme levels as well as the elevation of LC3b and ROS levels. In conclusion, the mitochondrial TCA cycle is affected by the inflammatory environment, and the LPS-induced effects can be reversed by Met treatment.
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