ArticleMilitary Medical Research2022
Celastrol mitigates inflammation in sepsis by inhibiting the PKM2-dependent Warburg effect.
Article in Military Medical Research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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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.
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Who cites it
73 citing papers in PubMed, 92 citations in OpenAlex.
- 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
- Lactate-Induced K370 Lactylation of STING Inhibits STING-TBK1 Signaling and Dampens Anti-Tumor Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Senkyunolide I Inhibits mtDNA-cGAS-STING Signaling in Macrophages via Targeting VDAC1 Oligomerization to Attenuate Ulcerative Colitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- PKM2: A gatekeeper in macrophage metabolic reprogramming.Journal of pharmaceutical analysis · 2026Review
- Engineering oral celastrol-polysaccharide supramolecular nanoassemblies across intestinal barriers for the intervention of nonalcoholic steatohepatitis.Materials today. Bio · 2026Article
- Death-associated protein kinase 2 (DAPK2) propagates endoplasmic reticulum stress in macrophages to worsen sepsis through HSPA5-IRE1α axis.Molecular biomedicine · 2026Article
- Macrophage immunometabolism in stroke: a view from single-cell and nano technologies.Journal of translational medicine · 2026Review
- Review
- Lactylation: a promising target for musculoskeletal disorders via interactions with chronic inflammation.Journal of advanced research · 2026Review
- Bench-to-Bedside Insights into the Challenges of Immunosuppression in Sepsis.Pathogens (Basel, Switzerland) · 2026Review
- Icaritin Ameliorates Cisplatin-Induced Mitochondrial Metabolic Dysfunction-Associated Nephrotoxicity and Synergistically Potentiates Its Antitumor Efficacy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Genome-wide CRISPR screening identifiesOncology letters · 2026Article
- Chemoproteomics-based profiling elucidates the antimalarial effects of amodiaquine through disruption of glycolysis process in Plasmodium falciparum.Cell communication and signaling : CCS · 2026Article
- Crosstalk of regulated cell death pathways in sepsis-associated acute kidney injury: implications for therapy.Frontiers in cell and developmental biology · 2026Review
- Dahuang-mudanpi decoction mitigates ALI/ARDS pulmonary inflammation via multi-target regulation of HMGB1.Frontiers in pharmacology · 2026Article
- Screening and Targeting the HMGB1/RAGE Axis via Proteomics to Alleviate Inflammatory Responses in aJournal of inflammation research · 2026Article
- Effect of PKM2 onFrontiers in cellular and infection microbiology · 2026Article
- Nanobody Nb07 mitigates sepsis by blocking the PFKM-p53-PD-1 axis to enhance macrophage phagocytosis.Theranostics · 2026Article
- Integrated single-cell transcriptomics and proteomics elucidate the molecular mechanisms and detoxification strategy of rifampicin-induced hepatotoxicity.International journal of biological sciences · 2026Article
- Forsythoside E Alleviates Liver Injury by Targeting PKM2 Tetramerization to Promote Macrophage M2 Polarization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSepsis involves life-threatening organ dysfunction and is caused by a dysregulated host response to infection. No specific therapies against sepsis have been reported. Celastrol (Cel) is a natural anti-inflammatory compound that shows potential against systemic inflammatory diseases. This study aimed to investigate the pharmacological activity and molecular mechanism of Cel in models of endotoxemia and sepsis.
methodsWe evaluated the anti-inflammatory efficacy of Cel against endotoxemia and sepsis in mice and macrophage cultures treated with lipopolysaccharide (LPS). We screened for potential protein targets of Cel using activity-based protein profiling (ABPP). Potential targets were validated using biophysical methods such as cellular thermal shift assays (CETSA) and surface plasmon resonance (SPR). Residues involved in Cel binding to target proteins were identified through point mutagenesis, and the functional effects of such binding were explored through gene knockdown.
resultsCel protected mice from lethal endotoxemia and improved their survival with sepsis, and it significantly decreased the levels of pro-inflammatory cytokines in mice and macrophages treated with LPS (P < 0.05). Cel bound to Cys424 of pyruvate kinase M2 (PKM2), inhibiting the enzyme and thereby suppressing aerobic glycolysis (Warburg effect). Cel also bound to Cys106 in high mobility group box 1 (HMGB1) protein, reducing the secretion of inflammatory cytokine interleukin (IL)-1β. Cel bound to the Cys residues in lactate dehydrogenase A (LDHA).
conclusionCel inhibits inflammation and the Warburg effect in sepsis via targeting PKM2 and HMGB1 protein.
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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 OpenQuestion graph.