ArticleJournal of the American Heart Association2025
CD11b Blockade Ameliorates Myocardial Ischemia/Reperfusion Injury by Reducing Neutrophil and Monocyte Infiltration.
Article in Journal of the American Heart Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Galectin-9Aging cell · 2026Article
- Monocyte-mediated mechanisms in idiopathic pulmonary fibrosis: opportunities for early intervention.Apoptosis : an international journal on programmed cell death · 2026Review
- The role of macrophage polarization in organ transplantation: research progress on impact on graft injury, repair, and fibrosis.Frontiers in immunology · 2026Review
- Article
- Neutrophil-mediated myocardial ischemia-reperfusion injury: mechanisms and potential therapeutic targets.Frontiers in immunology · 2026Review
- CD11b-modified ROS/pH-responsive nanoparticles co-deliver Dioscin and siRNA to improve cardiac repair after myocardial infarction by reducing neutrophil recruitment.Materials today. Bio · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMyocardial ischemia/reperfusion (I/R) injury is a leading cause of myocardial dysfunction and is associated with inflammation, apoptosis, and fibrosis. The integrin subunit ITGAM (also known as CD11b) mainly mediates leukocyte infiltration in the inflammatory process. However, the importance of CD11b in the development of myocardial I/R injury is unclear. The goal of this study is to investigate the role of CD11b
methodsWild-type mice were administered an anti-CD11b neutralizing antibody before myocardial I/R surgery. Echocardiography and histological staining were used to evaluate cardiac function and injury, respectively. Inflammatory cells were analyzed by flow cytometry in mice and patients with myocardial infarction who underwent percutaneous coronary intervention. Activated fibroblasts from patients with myocardial infarction were detected by positron emission tomography/computed tomography with a [(18)F]-labeled fibroblast activation protein inhibitor.
resultsOur results indicated that CD11b expression and the number of CD45
conclusionsOur data demonstrate that CD11b plays an important role in promoting myocardial I/R injury through multiple signaling pathways and that targeting CD11b may represent a promising option for treating heart I/R injury.
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