ArticleChinese medicine2026
Celastrol ameliorates atherosclerosis by inhibiting TLR4/STAT3/NLRP3-mediated macrophage pyroptosis.
Article in Chinese medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Celastrol Attenuates Doxorubicin-Induced Heart Failure by Preserving Mitochondrial Integrity and Suppressing Oxidative Stress and Is Accompanied by Changes in Gut Microbiota.Pharmaceuticals (Basel, Switzerland) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
backgroundAtherosclerosis is a chronic inflammatory disease characterized by plaque formation. Macrophage pyroptosis critically contributes to the formation and expansion of necrotic core as well as the instability of atherosclerotic plaque. Celastrol is a pentacyclic triterpene derived from the root of Tripterygium wilfordii Hook F, which has powerful anti-inflammatory properties. This study aimed to explore the effect and mechanism of celastrol in preventing atherosclerosis by regulating macrophage pyroptosis.
methodsAn atherosclerotic mouse model in vivo and a macrophage pyroptosis model induced by ox-LDL in vitro were established successfully. The cell viability was examined by CCK-8. The role of pyroptosis was detected by transmission electron microscopy, LDH assay, and PI staining. HE staining assay was applied to evaluate the morphology of vascular tissues. The degree of lipid accumulation in plaques was measured using Oil Red O staining. The collagen content of plaques was detected using Masson staining. Western blot analysis, RT-qPCR, immunofluorescence staining, and immunohistochemistry were used to determine the levels of key proteins related to pyroptosis in macrophages. The underlying target of celastrol was investigated by CETSA and SPR assays.
resultsOx-LDL effectively activated macrophage pyroptosis, which was markedly inhibited by celastrol in vitro. Consistently, celastrol suppressed atherosclerotic plaque progression and instability in apoE
conclusionThe present study demonstrates for the first time that celastrol prevents macrophage pyroptosis by inhibiting TLR4/STAT3/NLRP3 signaling pathway, ultimately alleviating atherosclerosis. These findings indicate that celastrol can serve as a potential therapeutic drug for atherosclerosis.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.