ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2025
Mediation of macrophage M1 polarization dynamics change by ubiquitin-autophagy-pathway regulated NLRP3 inflammasomes in PD-1 inhibitor-related myocardial inflammatory injury.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Avoidance of cardiac toxicity during the application of immune checkpoint inhibitors: a safety systematic review combining network meta-analysis and pharmacovigilance study.Frontiers in immunology · 2026Pooled it
- PD-1/PD-L1 inhibitor induces systemic inflammation and alters cardiac lipid metabolism in C57BL/6 J mice.Human cell · 2026Article
- Heterogeneity of macrophages in PD-1/PD-L1 inhibitor therapy: a single-cell perspective.Cellular & molecular biology letters · 2026Review
- Decoding the Cardiac Immune Microenvironment and Fibroblast Crosstalk in Radiotherapy Combined with Immunotherapy-Induced Cardiac Fibrosis Based on Single-Cell Transcriptomic Analysis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Pathological mechanisms and treatment strategies for immune checkpoint inhibitor-associated myocarditis: insights from single-cell sequencing.Basic research in cardiology · 2026Review
- MCC950-Loaded M12-Liposome Nanoparticles for Targeted Inhibition of NLRP3 Inflammasome in Sepsis-Induced Muscle Atrophy.Journal of cachexia, sarcopenia and muscle · 2026Article
- Evidence of Cardiotoxic Immune Activation by Triple Immune Checkpoint Blockade: A Translational Alert for Clinical Surveillance in Patients With Cancer.Journal of cardiovascular pharmacology · 2026Article
- Macrophage polarization in inflammatory regulation: molecular mechanisms, therapeutic targets, and translational challenges.Cellular and molecular life sciences : CMLS · 2026Review
- Immune checkpoint inhibition and heart injury: molecular mechanisms and clinical challenges.ESC heart failure · 2026Review
- Cardiovascular toxicity induced by immune checkpoint inhibitors: mechanisms linking immune dysregulation and myocardial fibrosis.American journal of clinical and experimental immunology · 2026Review
- Mechanisms and biomarkers of immune checkpoint inhibitor-associated myocarditis: from T cell imbalance to multicellular crosstalk.Frontiers in immunology · 2026Review
- Deciphering Cancer Therapy-Induced Cardiotoxicity in the Era of Spatial and Multi-Omics from Systemic Mechanisms toJournal of Cancer · 2026Review
- Omics-based biomarkers of immune-related organ toxicities associated with immune checkpoint inhibitors: a scoping review and evidence map.Frontiers in immunology · 2026Article
- Role of innate immunity in the development of cancer immunotherapy immune-mediated adverse events.Frontiers in immunology · 2026Review
- USP39 inhibits MLKL phosphorylation and deubiquitination to suppress necroptosis of nucleus pulposus cells and attenuate intervertebral disc degeneration.Journal of orthopaedic translation · 2026Article
- Role of the NLRP3 inflammasome in diabetes and its complications (Review).Molecular medicine reports · 2025Review
- The Role of Autophagy in HIV Infection and Immunological Recovery of ART-Treated PLWH.Viruses · 2025Review
- The Ubiquitin-Proteasome System: A Key Regulatory Hub in Myocarditis Leading to Dilated Cardiomyopathy.Journal of inflammation research · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
OBJECTIVE AND
designImmune checkpoint inhibitors (ICIs)-induced cardiac injury is a life-threatening immune-related adverse events (irAEs). However, the current understanding of its pathogenesis and therapeutic options is relatively limited. We aimed to provide a comprehensive overview of the myocardial inflammatory injury process and underlying mechanisms associated with ICIs. MATERIAL OR SUBJECTS: We conducted a descriptive analysis of lung cancer patients with ICIs-induced myocarditis at our institution and validated our clinical findings using single-cell sequencing (scRNA-seq) data. Furthermore, we established animal and cellular models to investigate the underlying mechanisms.
resultsOur findings revealed that lung cancer patients with ICIs-induced myocarditis exhibit an early increase in peripheral blood monocytes, which migrate to the heart and differentiate into macrophages, ultimately leading to myocardial inflammation. Mechanistically, programmed death-1 (PD-1) inhibition triggers myocardial inflammation through the activation of the signal transducer and activator of transcription 1 (STAT1)/nuclear factor kappa-B (NF-κB)/oligomerization domain (NOD)-like receptor thermal protein domain-associated protein 3 (NLRP3) signaling pathway and drives the polarization of macrophages towards the M1 phenotype. However, the ubiquitin (Ub)-autophagy pathway degrades NLRP3 inflammasomes, resulting in the gradual resolution of inflammation and the transition of M1 macrophages to the M2 phenotype. Finally, mouse experiments confirmed that NLRP3 inhibition using MCC950 effectively alleviates myocardial inflammatory injury.
conclusionsWe recommend monitoring fluctuations in peripheral blood monocyte counts in lung cancer patients undergoing ICIs treatment. Additionally, MCC950 holds potential as a therapeutic agent for ICIs-induced cardiac inflammation injury.
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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.