ArticleJournal for immunotherapy of cancer2025
Targeting the NLRP3 inflammasome abrogates cardiotoxicity of immune checkpoint blockers.
Article in Journal for immunotherapy of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Cardiovascular Risk Stratification and Surveillance in Cardio-Oncology: Mechanistic Foundations and Future Directions.Biomedicines · 2026Review
- Cardioimmunology of Myocarditis: Targeting the IL-1 Pathway.Current cardiology reports · 2026Review
- Pembrolizumab-Associated Serositis With Recurrent Pleural Effusions Successfully Treated With Anakinra.Clinical case reports · 2026Article
- Interaction between Regulated Cell Death Pathways and Core Cellular Processes: Unraveling the Molecular Mechanisms of Cardiotoxicity of Antitumor Drugs.Current treatment options in oncology · 2026Review
- Caught in the crossfire: cardiac complications of cancer therapy.The Journal of clinical investigation · 2026Review
- Role of innate immunity in the development of cancer immunotherapy immune-mediated adverse events.Frontiers in immunology · 2026Review
- Single-cell transcriptomic insights into the immune heterogeneity of immune checkpoint inhibitors related organ toxicities.Frontiers in immunology · 2026Review
- The NLRP3 inflammasome in gynecological cancers: a double-edged sword shaping the immune microenvironment and immunotherapy response.Frontiers in immunology · 2026Review
- Cardiovascular toxicity induced by immune checkpoint inhibitors: mechanisms linking immune dysregulation and myocardial fibrosis.American journal of clinical and experimental immunology · 2026Review
- Targeting NLRP3 Inflammasomes in Myocarditis: Potential Therapeutic Strategies and Clinical Translation.Scientifica · 2026Review
- NLRP3 inflammasomes at the ARDS-cancer interface: mechanisms and translational hypotheses.Frontiers in immunology · 2026Review
- NLRPs and tumor: research progress from molecular mechanisms to clinical applications.Oncogene · 2026Review
- Immune checkpoint inhibitors and cardiovascular toxicity: immunology, pathophysiology, diagnosis, and management.Journal of thrombosis and thrombolysis · 2025Review
- Liraglutide attenuates autoimmune myocarditis by inhibiting NLRP3 and NF-κb pathways.Scientific reports · 2025Article
- NLRP3 inflammasome: structure, mechanism, drug-induced organ toxicity, therapeutic strategies, and future perspectives.RSC medicinal chemistry · 2025Review
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundImmune checkpoint inhibitors (ICIs) have revolutionized the treatment of many malignant tumors. However, ICI-induced hyper-immune activation causes cardiotoxicity. Traditional treatments such as glucocorticoids and immunosuppressants have limited effectiveness and may even accelerate tumor growth. This study aimed to identify approaches that effectively reduce cardiotoxicity and simultaneously preserve or enhance the antitumor immunity of ICI therapy.
methodsICI injection in melanoma-bearing C57BL/6J female mice was used to simulate cardiotoxicity in patients with tumor undergoing immune therapy. MCC950 was used to block nod-like receptor protein 3 (NLRP3) inflammasome activity. Echocardiography, immunofluorescence, flow cytometry, and reverse transcription quantitative polymerase chain reaction were used to assess cardiac function, immune cell populations, and inflammatory factor levels. Bulk and single-cell RNA sequencing was used to detect the changes in cardiac transcriptome and immunological network.
resultsNLRP3 inhibition reduced inflammatory response and improved cardiac function. Notably, NLRP3 inhibition also resulted in a pronounced suppression of tumor growth. Single-cell RNA sequencing elucidated that MCC950 treatment reduced the cardiac infiltration of pathogenic macrophages, cytotoxic T cells, activated T cells, and their production of inflammatory cytokines, while enhancing the presence of reparative macrophages and naive T cells. In addition, MCC950 attenuated cardiotoxicity induced by dual programmed cell death protein 1 (PD-1) and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) immunotherapy and promoted tumor regression, and showed efficacy in treating established cardiotoxicity.
conclusionsOur findings provide a promising clinical approach for preventing and treating cardiotoxicity induced by ICIs, dissociating the antitumor efficacy of ICI-based therapies from their cardiotoxic side effects.
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