ArticleCell death discovery2019
Celastrol attenuates ox-LDL-induced mesangial cell proliferation via suppressing NLRP3 inflammasome activation.
Article in Cell death discovery, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- Effects of chronic jetlag on high-fat and high-fructose diet induced renal injury in mice.Scientific reports · 2026Article
- USP16 drives psoriasis progression by deubiquitinating and stabilizing NLRP3 in keratinocytes.JCI insight · 2026Article
- Ectopic lipid deposition in kidney diseases: mechanisms in specific cell types and therapeutic strategies.Frontiers in endocrinology · 2026Review
- Targeting the NLRP3 inflammasome with natural products for ischemia-reperfusion injury across organs: mechanisms, structure-activity relationships, and delivery innovations.Inflammopharmacology · 2025Review
- Celastrol alleviates esophageal stricture in rats by inhibiting NLR family pyrin domain containing 3 activation.World journal of gastroenterology · 2025Article
- The role of celastrol in inflammation and diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Mechanistic study of celastrol-mediated inhibition of proinflammatory activation of macrophages in IgA nephropathy via down-regulating ECM1.International journal of biological sciences · 2024Article
- Network Pharmacology and Experimental Validation to Explore That Celastrol Targeting PTEN is the Potential Mechanism ofDrug design, development and therapy · 2023Article
- Oncostatin M promotes the ox-LDL-induced activation of NLRP3 inflammasomes via the NF-κB pathway in THP-1 macrophages and promotes the progression of atherosclerosis.Annals of translational medicine · 2022Article
- Therapeutic regulation of the NLRP3 inflammasome in chronic inflammatory diseases.Archives of pharmacal research · 2021Review
- Regulation of the NLRP3 Inflammasome by Post-Translational Modifications and Small Molecules.Frontiers in immunology · 2020Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mesangial cell (MC) proliferation is one of the important pathological features of obesity-associated nephropathy with unknown etiology. Excessive MC proliferation can cause glomerulosclerosis and renal function loss. Thus, targeting MC proliferation may be a potential strategy for the treatment of obesity-associated kidney disease. The present study was undertaken to investigate the role of celastrol in MC proliferation induced by ox-LDL, as well as the potential mechanisms. Following ox-LDL treatment, MC proliferation was induced and the NLRP3 inflammasome was activated, as evidenced by increased NLRP3 levels, caspase 1 activity, and IL-18 and IL-1β release. Significantly, NLRP3 siRNAs inhibited MC proliferation and delayed cell cycle progression, as indicated by the cell cycle assay and the expression of cyclin A2 and cyclin D1. Given the anti-inflammatory effect of celastrol, we pretreated MCs with celastrol before ox-LDL treatment. As expected, celastrol pretreatment strikingly inhibited NLRP3 inflammasome activation and MC proliferation triggered by ox-LDL. In summary, celastrol potently blocked ox-LDL-induced MC proliferation, possibly by inhibiting NLRP3 inflammasome activation. These findings also suggest that celastrol may be a potential drug for treating proliferative glomerular diseases related to obesity and lipid disorders.
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