ArticleSignal transduction and targeted therapy2022
CB1R-stabilized NLRP3 inflammasome drives antipsychotics cardiotoxicity.
Article in Signal transduction and targeted therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- Protective effect of Guanxinning on antipsychotic-induced cardiac impairment in long-term hospitalized psychiatric patients.World journal of psychiatry · 2026Trial
- Stanniocalcin-1 Attenuates Cardiac Fibrosis Post Ischemia-Reperfusion Injury by Targeting the DOCKER Domain of Dedicator of Cytokinesis 1.Journal of the American Heart Association · 2026Article
- Multi-Target Cardioprotective Potential of Garcinia indica Choisy in Olanzapine-Induced Cardiometabolic Dysregulation: Evidence From Computational and Experimental Insights in H9c2(2-1) Cells.Chemistry & biodiversity · 2026Article
- Subthreshold Thermal Stress Aggravates Methamphetamine-Induced Cardiomyocyte Pyroptosis via the Mitochondrial ROS/BAX/mtDNA/NLRP3 Pathway.International journal of molecular sciences · 2026Article
- Targeting Cold-Inducible RNA-Binding Protein Attenuates Pancreatic Fibrosis by Suppressing Pyroptosis in Chronic Pancreatitis.Inflammation · 2026Article
- NPM3 functions as a lactyltransferase to promote necroptosis in male diabetic cardiomyopathy mice models via FASN transcription modulation.Nature communications · 2026Article
- BACH2 alleviates immune checkpoint inhibitors-induced cardiac pyroptosis via transcriptionally promoting GRSF1.Clinical and translational medicine · 2026Article
- Forensic postmortem findings for sudden unexplained death in schizophrenia: case series and literature review.Frontiers in psychiatry · 2026Article
- GLUT5-Mediated Disruption of the Gut-Testis Axis Deteriorates Olanzapine-Induced Testicular Fibrosis and is Ameliorated by Dapagliflozin.Drug design, development and therapy · 2026Article
- FGF9 alleviates diabetic cardiomyopathy by activating Nrf2 via SQSTM1/p62-Keap1 in mice.Communications biology · 2025Article
- Targeting Zfp36 to combat cardiac hypertrophy: Insights into ferroptosis pathways.Clinical and translational medicine · 2025Article
- Global Research Trends and Focus on the Link Between Heart Failure and NLRP3 Inflammasome: A Bibliometric Analysis From 2010 to 2024.Journal of multidisciplinary healthcare · 2025Review
- Exploration of Clozapine-Induced Cardiomyopathy and Its Mechanism.Cardiovascular toxicology · 2024Article
- Pyroptosis in health and disease: mechanisms, regulation and clinical perspective.Signal transduction and targeted therapy · 2024Review
- Article
- Cannabidiol ameliorates lipopolysaccharide-induced cardiovascular toxicity by its antioxidant and anti-inflammatory activity via regulating IL-6, Hif1α, STAT3, eNOS pathway.Molecular biology reports · 2024Article
- The role of inflammasomes in human diseases and their potential as therapeutic targets.Signal transduction and targeted therapy · 2024Review
- The scheme, and regulative mechanism of pyroptosis, ferroptosis, and necroptosis in radiation injury.International journal of biological sciences · 2024Review
- Targeting NLRP3 inflammasome for neurodegenerative disorders.Molecular psychiatry · 2023Review
- Adverse effects of tyrosine kinase inhibitors in cancer therapy: pathophysiology, mechanisms and clinical management.Signal transduction and targeted therapy · 2023Review
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long-term use of antipsychotics is a common cause of myocardial injury and even sudden cardiac deaths that often lead to drug withdrawn or discontinuation. Mechanisms underlying antipsychotics cardiotoxicity remain largely unknown. Herein we performed RNA sequencing and found that NLRP3 inflammasome-mediated pyroptosis contributed predominantly to multiple antipsychotics cardiotoxicity. Pyroptosis-based small-molecule compound screen identified cannabinoid receptor 1 (CB1R) as an upstream regulator of the NLRP3 inflammasome. Mechanistically, antipsychotics competitively bond to the CB1R and led to CB1R translocation to the cytoplasm, where CB1R directly interacted with NLRP3 inflammasome via amino acid residues 177-209, rendering stabilization of the inflammasome. Knockout of Cb1r significantly alleviated antipsychotic-induced cardiomyocyte pyroptosis and cardiotoxicity. Multi-organ-based investigation revealed no additional toxicity of newer CB1R antagonists. In authentic human cases, the expression of CB1R and NLRP3 inflammasome positively correlated with antipsychotics-induced cardiotoxicity. These results suggest that CB1R is a potent regulator of the NLRP3 inflammsome-mediated pyroptosis and small-molecule inhibitors targeting the CB1R/NLRP3 signaling represent attractive approaches to rescue cardiac side effects of antipsychotics.
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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.