ArticleCardiovascular research2010
CB1 cannabinoid receptors promote oxidative stress and cell death in murine models of doxorubicin-induced cardiomyopathy and in human cardiomyocytes.
Article in Cardiovascular research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.
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Who cites it
107 citing papers in PubMed, 196 citations in OpenAlex.
- Tissue-specific roles of monoacylglycerol (MAG) in metabolic diseases.Immunometabolism (Cobham, Surrey) · 2026Review
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- Synthetic Cannabinoid AB-FUBINACA Negatively Impacted the Male Fertility and Induced Testicular Toxicity.Forensic toxicology · 2026Article
- Selective Depletion of Gut Gram-Negative Bacteria Attenuates Alcohol Binge-Induced Cardiovascular Dysfunction by Lowering Cardiac Anandamide Levels.The American journal of pathology · 2026Article
- Kinin B1 receptor mediates acute cardiovascular and neural responses following cannabinoid receptor 1 activation in conscious male mice.Physiological reports · 2025Article
- Ring Finger Protein 2 Promotes Oxidative Stress and Mitochondrial Dysfunction in Doxorubicin-Induced Cardiotoxicity Via the Mercaptopyruvate Sulfurtransferase/Hydrogen Sulfide Pathway.Journal of the American Heart Association · 2025Article
- ELABELA-32 Alleviates Doxorubicin-Induced Chronic Cardiotoxicity by Inhibiting the TGF-β/Smad Signaling Pathway.Cardiovascular toxicology · 2025Article
- The relationship between cannabis and cardiovascular disease: clearing the haze.Nature reviews. Cardiology · 2025Review
- Exacerbated cardiac dysfunction from combined alcohol binge and synthetic cannabinoid use.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Article
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- Tetrahedral Framework Nucleic Acids Inhibit Oxidative Stress and Cardiomyocyte Apoptosis in Doxorubicin-Induced Cardiotoxicity.International journal of nanomedicine · 2025Article
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- Cardiomyocyte-specific knockout of ADAM17 alleviates doxorubicin-induced cardiomyopathy via inhibiting TNFα-TRAF3-TAK1-MAPK axis.Signal transduction and targeted therapy · 2024Article
- Nicotinamide Mononucleotide Supplementation Alleviates Doxorubicin-Induced Multi-Organ Fibrosis.International journal of molecular sciences · 2024Article
- Applications of Cannabinoids in Neuropathic Pain: An Updated Review.Critical reviews in therapeutic drug carrier systems · 2024Review
- Role of Cannabinoid Signaling in Cardiovascular Function and Ischemic Injury.The Journal of pharmacology and experimental therapeutics · 2023Review
- Role of CB1 Cannabinoid Receptors in Vascular Responses and Vascular Remodeling of the Aorta in Female Mice.International journal of molecular sciences · 2023Article
- Effects of the CB1 receptor antagonists AM6545 and AM4113 on metabolic syndrome-induced prostatic hyperplasia in rats.Biomolecules & biomedicine · 2023Article
- Crosstalk between Exercise-Derived Endocannabinoidome and Kynurenines: Potential Target Therapies for Obesity and Depression Symptoms.Pharmaceuticals (Basel, Switzerland) · 2023Review
47 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
aimsHere we investigated the mechanisms by which cardiovascular CB1 cannabinoid receptors may modulate the cardiac dysfunction, oxidative stress, and interrelated cell death pathways associated with acute/chronic cardiomyopathy induced by the widely used anti-tumour compound doxorubicin (DOX). METHODS AND
resultsBoth load-dependent and -independent indices of left-ventricular function were measured by the Millar pressure-volume conductance system. Mitogen-activated protein kinase (MAPK) activation, cell-death markers, and oxidative/nitrosative stress were measured by molecular biology/biochemical methods and flow cytometry. DOX induced left-ventricular dysfunction, oxidative/nitrosative stress coupled with impaired antioxidant defense, activation of MAPK (p38 and JNK), and cell death and/or fibrosis in hearts of wide-type mice (CB1(+/+)), and these effects were markedly attenuated in CB1 knockouts (CB1(-/-)). In human primary cardiomyocytes expressing CB1 receptors (demonstrated by RT-PCR, western immunoblot, and flow cytometry) DOX, likewise the CB1 receptor agonist HU210 and the endocannabinoid anandamide (AEA), induced MAPK activation and cell death. The DOX-induced MAPK activation and cell death were significantly enhanced when DOX was co-administered with CB1 agonists AEA or HU210. Remarkably, cell death and MAPK activation induced by AEA, HU210, and DOX +/- AEA/HU210 were largely attenuated by either CB1 antagonists (rimonabant and AM281) or by inhibitors of p38 and JNK MAPKs. Furthermore, AEA or HU210 in primary human cardiomyocytes triggered increased reactive oxygen species generation.
conclusionCB1 activation in cardiomyocytes may amplify the reactive oxygen/nitrogen species-MAPK activation-cell death pathway in pathological conditions when the endocannabinoid synthetic or metabolic pathways are dysregulated by excessive inflammation and/or oxidative/nitrosative stress, which may contribute to the pathophysiology of various cardiovascular diseases.
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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.