ArticleScience translational medicine2020
Blocking the death checkpoint protein TRAIL improves cardiac function after myocardial infarction in monkeys, pigs, and rats.
Article in Science translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
- Review
- Cardiac reprogramming via transient overexpression of P-glycoprotein alleviates doxorubicin-induced cardiotoxicity in mice and pigs.Nature communications · 2026Article
- Ion channels and cardiac disease: mechanisms and functions of a disintegrin and metalloproteases and their substrates.Frontiers in cell and developmental biology · 2026Review
- Blocking the TRAIL-DR5 Pathway Reduces Cardiac Ischemia-Reperfusion Injury by Decreasing Neutrophil Infiltration and Neutrophil Extracellular Traps Formation.Cardiovascular drugs and therapy · 2025Article
- Exploratory Study of Prognostic Plasma Biomarkers in Patients with Pulmonary Arterial Hypertension.The American journal of pathology · 2025Article
- Apoptosis in Cardiac Conditions Including Cirrhotic Cardiomyopathy.International journal of molecular sciences · 2025Review
- ROS-responsive death receptor 5 fusion protein nano-delivery system enhances myocardial ischemia-reperfusion injury protection.Materials today. Bio · 2025Article
- Cardiac rehabilitation in porcine models: Advances in therapeutic strategies for ischemic heart disease.Zoological research · 2025Review
- Spatiotemporal transcriptomics elucidates the pathogenesis of fulminant viral myocarditis.Signal transduction and targeted therapy · 2025Article
- Cardiorenal protective effects of Tanhuo decoction in acute myocardial infarction via regulating multi-target inflammation and metabolic signaling pathways.Frontiers in pharmacology · 2025Article
- Advances in the study of death receptor 5.Frontiers in pharmacology · 2025Review
- The Dual Role of the TRAIL-DR5 Signaling Axis in Cardiovascular Disease: From Molecular Mechanisms to Targeted Therapies.Biologics : targets & therapy · 2025Review
- Ion cocktail therapy for myocardial infarction by synergistic regulation of both structural and electrical remodeling.Exploration (Beijing, China) · 2024Article
- Recovering intestinal redox homeostasis to resolve systemic inflammation for preventing remote myocardial injury by oral fullerenes.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Microarray Analysis for Transcriptomic Profiling of Myocardium in Patients with Fatal Myocardial Infarction.Biomedicines · 2023Article
- The Prognostic, Diagnostic, and Therapeutic Potential of TRAIL Signalling in Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- Tumor Necrosis Factor Family Members and Myocardial Ischemia-Reperfusion Injury: State of the Art and Therapeutic Implications.International journal of molecular sciences · 2023Review
- A Pharmacological Review of Tanshinones, Naturally Occurring Monomers fromOxidative medicine and cellular longevity · 2023Review
- TRAIL and its receptors in cardiac diseases.Frontiers in physiology · 2023Review
- Blocking TRAIL-DR5 signaling pathway with soluble death receptor 5 fusion protein mitigates radiation-induced injury.Frontiers in pharmacology · 2023Article
Corrections and comments
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Authors and funding
43 authors at 4 institutions in 2 countries.
Funding
Abstract
Myocardial infarction (MI) is a leading cause of death worldwide for which there is no cure. Although cardiac cell death is a well-recognized pathological mechanism of MI, therapeutic blockade of cell death to treat MI is not straightforward. Death receptor 5 (DR5) and its ligand TRAIL [tumor necrosis factor (TNF)-related apoptosis-inducing ligand] are up-regulated in MI, but their roles in pathological remodeling are unknown. Here, we report that blocking TRAIL with a soluble DR5 immunoglobulin fusion protein diminished MI by preventing cardiac cell death and inflammation in rats, pigs, and monkeys. Mechanistically, TRAIL induced the death of cardiomyocytes and recruited and activated leukocytes, directly and indirectly causing cardiac injury. Transcriptome profiling revealed increased expression of inflammatory cytokines in infarcted heart tissue, which was markedly reduced by TRAIL blockade. Together, our findings indicate that TRAIL mediates MI directly by targeting cardiomyocytes and indirectly by affecting myeloid cells, supporting TRAIL blockade as a potential therapeutic strategy for treating MI.
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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.