ArticleTheranostics2020
CD226 deletion improves post-infarction healing via modulating macrophage polarization in mice.
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Article in Theranostics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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29citing papers in PubMed
4.3field-weighted citation impact, top 4% of its field
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Who cites it
29 citing papers in PubMed, 42 citations in OpenAlex.
- CD226 Deficiency Attenuates Periodontal Bone Destruction in a Murine Ligature-Induced Periodontitis Model.Biology · 2026Article
- Interleukin enhancer binding factor 3 exacerbates cardiac inflammation and injury following myocardial infarction by inhibiting Lys48-linked ubiquitination on HNRNPA2B1 in macrophages.Cellular & molecular immunology · 2026Article
- Inhibition of macrophage migration inhibitory factor attenuates bleomycin-induced murine pulmonary fibrosis via the MAPK pathway.Respiratory research · 2026Article
- The impact of natural and engineered extracellular vesicles on post-myocardial infarction angiogenesis.Stem cell research & therapy · 2025Review
- Alpha-ketoglutarate protects against myocardial infarction via FTO-mediated anti-inflammatory macrophage activation.Basic research in cardiology · 2025Article
- The Immune Regulatory Functions of CD226 and Its Implications in Immune-Mediated Diseases.Biomolecules · 2025Review
- Advancements in macrophage research for cardiovascular disease.Frontiers in physiology · 2025Review
- FOS as a biomarker for myocardial infarction treatment with Deng's Yangxin Decoction: a systems biology-based analysis.Frontiers in cardiovascular medicine · 2025Article
- M2 macrophage-derived exosomes promote angiogenesis and improve cardiac function after myocardial infarction.Biology direct · 2024Article
- Platelet Membrane Nanocarriers Cascade Targeting Delivery System to Improve Myocardial Remodeling Post Myocardial Ischemia-Reperfusion Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Montelukast, an available and safe anti-asthmatic drug, prevents maladaptive remodelling and maintains cardiac functionality following myocardial infarction.Scientific reports · 2024Article
- Macrophage neogenin deficiency exacerbates myocardial remodeling and inflammation after acute myocardial infarction through JAK1-STAT1 signaling.Cellular and molecular life sciences : CMLS · 2023Article
- The Role of M1 and M2 Myocardial Macrophages in Promoting Proliferation and Healing via Activating Epithelial-to-Mesenchymal Transition.Biomedicines · 2023Article
- Macrophages in the Inflammatory Phase following Myocardial Infarction: Role of Exogenous Ubiquitin.Biology · 2023Review
- Macrophages in cardiac remodelling after myocardial infarction.Nature reviews. Cardiology · 2023Review
- Microtomographic, histomorphometric, and molecular features show a normal alveolar bone healing process in iNOS-deficient mice along a compensatory upregulation of eNOS and nNOS isoforms.Journal of applied oral science : revista FOB · 2023Article
- Dynamic of Circulating DNAM-1+ Monocytes and NK Cells in Patients with STEMI Following Primary Percutaneous Coronary Intervention.Journal of cardiovascular development and disease · 2022Article
- Expression of CD226 is upregulated on Tr1 cells from neuromyelitis optica spectrum disorder patients.Brain and behavior · 2022Article
- Engineered neutrophil apoptotic bodies ameliorate myocardial infarction by promoting macrophage efferocytosis and inflammation resolution.Bioactive materials · 2022Article
- The Scientific Rationale for the Introduction of Renalase in the Concept of Cardiac Fibrosis.Frontiers in cardiovascular medicine · 2022Review
Corrections and comments
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Authors and funding
19 authors at 1 institution in 1 country.
Jun LiDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, School of Basic Medicine, Fourth Military Medical University, No.169, West Changle Road, Xi'an, 710032, China.
Yun SongDepartment of Immunology, School of Basic Medicine, Fourth Military Medical University, No.169, West Changle Road, Xi'an, 710032, China.
Jing-Yi JinDepartment of Immunology, School of Basic Medicine, Fourth Military Medical University, No.169, West Changle Road, Xi'an, 710032, China.
Guo-Hua LiDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, School of Basic Medicine, Fourth Military Medical University, No.169, West Changle Road, Xi'an, 710032, China.
Yong-Zheng GuoDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, School of Basic Medicine, Fourth Military Medical University, No.169, West Changle Road, Xi'an, 710032, China.
Hong-Yu YiDepartment of Immunology, School of Basic Medicine, Fourth Military Medical University, No.169, West Changle Road, Xi'an, 710032, China.
Jin-Rui ZhangDepartment of Immunology, School of Basic Medicine, Fourth Military Medical University, No.169, West Changle Road, Xi'an, 710032, China.
Ya-Jie LuDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, School of Basic Medicine, Fourth Military Medical University, No.169, West Changle Road, Xi'an, 710032, China.
Jing-Long ZhangDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, School of Basic Medicine, Fourth Military Medical University, No.169, West Changle Road, Xi'an, 710032, China.
Cong-Ye LiDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, No.169, West Changle Road, Xi'an, 710032, China.
Chao GaoDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, No.169, West Changle Road, Xi'an, 710032, China.
Lu YangDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, School of Basic Medicine, Fourth Military Medical University, No.169, West Changle Road, Xi'an, 710032, China.
Feng FuDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, School of Basic Medicine, Fourth Military Medical University, No.169, West Changle Road, Xi'an, 710032, China.
Fu-Lin ChenFaculty of Medicine, Northwest University, No.229, Taibai Bei Road, Xi'an, 710069, China.
Shu-Miao ZhangDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, School of Basic Medicine, Fourth Military Medical University, No.169, West Changle Road, Xi'an, 710032, China.
Min JiaDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, School of Basic Medicine, Fourth Military Medical University, No.169, West Changle Road, Xi'an, 710032, China.
Guo-Xu ZhengDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, School of Basic Medicine, Fourth Military Medical University, No.169, West Changle Road, Xi'an, 710032, China.
Jian-Ming PeiDepartment of Physiology and Pathophysiology, National Key Discipline of Cell Biology, School of Basic Medicine, Fourth Military Medical University, No.169, West Changle Road, Xi'an, 710032, China.
Li-Hua ChenDepartment of Immunology, School of Basic Medicine, Fourth Military Medical University, No.169, West Changle Road, Xi'an, 710032, China.
Northwest University · CN
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages are essential for wound repair after myocardial infarction (MI). CD226, a member of immunoglobulin superfamily, is expressed on inflammatory monocytes, however, the role of CD226 in infarct healing and the effect of CD226 on macrophage remain unknown.
Indexed as
Ventricular RemodelingAnimalsAntigens, Differentiation, T-LymphocyteEndothelial CellsMacrophage ActivationMacrophagesMiceMice, Inbred C57BLMice, KnockoutMonocytesMyocardial InfarctionMyocardiumPhenotypeT Lineage-Specific Activation Antigen 1Wound HealingAntigens, Differentiation, T-LymphocyteT Lineage-Specific Activation Antigen 1healinginflammationmacrophagemyocardial infarctionpolarization
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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.