ArticleOxidative medicine and cellular longevity2022
Dynamin-Related Protein 1 Is Involved in Mitochondrial Damage, Defective Mitophagy, and NLRP3 Inflammasome Activation Induced by MSU Crystals.
Article in Oxidative medicine and cellular longevity, 2022. 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, 20 citations in OpenAlex.
- Immunometabolic Modulation of the Bone Marrow Niche by Bioactive Materials to Rescue Impaired Fracture Healing.Stem cell reviews and reports · 2026Review
- Potential mechanisms of natural products in improving gouty arthritis: Focusing on NLRP3 inflammasome regulation.Journal of pharmaceutical analysis · 2026Review
- Axonal regeneration and hyperglycemia in wound healing: a review on the role of activin A, TNFRSF10B, and Synaptophysin.Molecular biology reports · 2026Review
- Advances in the mechanisms of the NLRP3 inflammasome in sepsis‑induced cardiomyopathy and targeted therapeutic studies (Review).Molecular medicine reports · 2026Review
- Gouty arthritis model: delving into disease pathways and uncovering possible therapeutic targets.Frontiers in endocrinology · 2026Review
- The dynamin-related proteinFrontiers in plant science · 2026Article
- Tumor necrosis factor alpha triggers mitochondrial dysfunction and ROS-driven cytokine amplification in bovine fibroblast-like synoviocytes.Frontiers in veterinary science · 2026Article
- Intracellular Calcium Dysregulation: The Hidden Culprit in the Diabetes-Gout Nexus.Biomedicines · 2025Review
- PINK1 functions in mitophagy and mitochondrial homeostasis during mice oocyte maturation.Cell & bioscience · 2025Article
- NLRP3 Inflammasome-Mediated Pyroptosis in Osteoporosis: Osteoimmune Mechanisms and Therapeutic Targeting.Journal of cellular and molecular medicine · 2025Review
- Unleashing the potential of exercise: conquering cardiovascular disease by targeting inflammasome activation.European journal of medical research · 2025Review
- Exploring NLRP3-related phenotypic fingerprints in human macrophages using Cell Painting assay.iScience · 2025Article
- Assessing the association between the non-HDL to HDL cholesterol ratio and NAFLD in Chinese adults: concentrate on gout populations.Frontiers in nutrition · 2025Article
- L-Arginine supplementation as mitochondrial therapy in diabetic cardiomyopathy.Cardiovascular diabetology · 2024Article
- Aflatoxin B1 decreased flesh flavor and inhibited muscle development in grass carp (Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2024Article
- Exposing kinetic disparities between inflammasome readouts using time-resolved analysis.Heliyon · 2024Article
- Drp1: Focus on Diseases Triggered by the Mitochondrial Pathway.Cell biochemistry and biophysics · 2024Review
- NLRP3 inflammasome and pyroptosis in cardiovascular diseases and exercise intervention.Frontiers in pharmacology · 2024Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive generation of reactive oxygen species (ROS) has great impacts on MSU crystal-induced inflammation. Drp1-dependent mitochondrial fission is closely associated with mitochondrial ROS levels. However, whether Drp1 signaling contributes to MSU crystal-induced inflammation remains unclear. Mice bone marrow-derived macrophages (BMDMs) were primed with LPS and then stimulated with MSU suspensions for 12 h. The protein levels associated with mitochondrial dynamics, oxidative stress, and mitophagy were detected by Western blot. BMDMs were loaded with MitoTracker Green probe to detect mitochondrial morphology. To measure mitochondrial reactive oxygen species (ROS) and total ROS levels, cells were loaded, respectively, with MitoSOX and DHE probes. The effects of Mito-TEMPO, an antioxidant that targets the mitochondria or DRP1 inhibitor (Mdivi-1) on MSU crystal-induced peritonitis and arthritis mouse models, were evaluated. Our study revealed that MSU crystal stimulation resulted in elevation of mitochondrial fragmentation of BMDMs. Treatment with Mito-TEMPO or Drp1 knockdown significantly ameliorated the mitochondrial damage induced by MSU crystals. BMDMs exposure to MSU crystals increased the expression of auto/mitophagy marker proteins and promoted the fusion of mitophagosomes with lysosomes, leading to accumulation of mitolysosomes. Drp1 knockdown alleviated defective mitophagy and activation of the NLRP3 inflammasome in MSU crystal-treated BMDMs. This study indicates that there is crosstalk between mitochondrial ROS and Drp1 signaling in MSU crystal-induced inflammation. Drp1 signaling is involved in MSU crystal-induced mitochondrial damage, impaired mitophagy and NLRP3 inflammasome activation.
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