ArticleCardiovascular therapeutics2023
The Regulation Network of Glycerolipid Metabolism as Coregulators of Immunotherapy-Related Myocarditis.
Article in Cardiovascular therapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- The Cardio-Onco-Immune Axis: immunopathological mechanisms in the cardiac microenvironment of checkpoint inhibitor-induced myocarditis.Acta pharmacologica Sinica · 2026Review
- Therapeutic Immunomodulation in Cardiovascular Disease: Anti-inflammatory Strategies and Landmark Trials.Cureus · 2025Review
- Different chromatographic techniques and recent advancements for biomedical and pharmaceutical applications.Northern clinics of Istanbul · 2025Article
- Immunogenic cell death-related cancer-associated fibroblast clusters and prognostic risk model in cervical cancer.APL bioengineering · 2024Article
- Cardiovascular Biomarkers in Cardio-Oncology: Antineoplastic Drug Cardiotoxicity and Beyond.Biomolecules · 2024Review
- Systemic Characterization of the Gut Microbiota Profile after Single Mild Ischemic Stroke and Recurrent Stroke in Mice.Biomedicines · 2024Article
- LCP1 knockdown in monocyte-derived macrophages: mitigating ischemic brain injury and shaping immune cell signaling and metabolism.Theranostics · 2024Article
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Authors and funding
6 authors.
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Abstract
Background: To date, immunotherapy for patients with malignant tumors has shown a significant association with myocarditis. However, the mechanism of metabolic reprogramming changes for immunotherapy-related cardiotoxicity is still not well understood. Methods: The CD45 Results: The scRNA analysis shows that the T cell is the main regulatory cell subpopulation in the pathological progress of immunotherapy-related myocarditis. Mitochondrial regulation pathway significantly participated in pseudotime trajectory- (PTT-) related differential expressed genes (DEGs) in the T cell subpopulation. Additionally, both the gene set enrichment analysis (GSEA) of PTT-related DEGs and LC-MS/MS metabolomics analysis showed that mitochondrial-regulated glycerolipid metabolism plays a central role in metabolic reprogramming changes for immunotherapy-related cardiotoxicity. Finally, the hub-regulated protease of diacylglycerol kinase zeta (Dgkz) was significantly identified and widely played various roles in glycerolipid metabolism, oxidative phosphorylation, and lipid kinase activation. Conclusion: Mitochondrial-regulated glycerolipid metabolism, especially the DGKZ protein, plays a key role in the metabolic reprogramming of immunotherapy-related myocarditis.
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