ArticleDiabetes & vascular disease research2009
The mannose-binding lectin pathway is a significant contributor to reperfusion injury in the type 2 diabetic heart.
Article in Diabetes & vascular disease research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Shedding of membrane complement inhibitors CD59 and CD46 into the circulation is associated with poor prognosis in acute coronary syndrome patients: a cohort study.Journal of translational medicine · 2024Article
- The Lectin Pathway of the Complement System-Activation, Regulation, Disease Connections and Interplay with Other (Proteolytic) Systems.International journal of molecular sciences · 2024Review
- Cold exposure induces vaso-occlusion and pain in sickle mice that depend on complement activation.Blood · 2023Article
- MASP-2 and MASP-3 inhibitors block complement activation, inflammation, and microvascular stasis in a murine model of vaso-occlusion in sickle cell disease.Translational research : the journal of laboratory and clinical medicine · 2022Article
- Recent advances into the role of pattern recognition receptors in transplantation.Cellular immunology · 2020Review
- Murine T Cell Maturation Entails Protection from MBL2, but Complement Proteins Do Not Drive Clearance of Cells That Fail Maturation in the Absence of NKAP.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Be on Target: Strategies of Targeting Alternative and Lectin Pathway Components in Complement-Mediated Diseases.Frontiers in immunology · 2018Review
- Mannose-Binding Lectin Levels and Carotid Intima-Media Thickness in Type 2 Diabetic Patients.Journal of diabetes research · 2016Article
- Fibrinogen-specific antibody induces abdominal aortic aneurysm in mice through complement lectin pathway activation.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- The complement system in ischemia-reperfusion injuries.Immunobiology · 2012Review
- Endogenous and natural complement inhibitor attenuates myocardial injury and arterial thrombogenesis.Circulation · 2012Article
- Targeting mannose-binding lectin confers long-lasting protection with a surprisingly wide therapeutic window in cerebral ischemia.Circulation · 2012Article
- Mannose-binding lectin-associated serine protease-1 is a significant contributor to coagulation in a murine model of occlusive thrombosis.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Absence of mannose-binding lectin prevents hyperglycemic cardiovascular complications.The American journal of pathology · 2012Article
- Exaggerated neutrophil-mediated reperfusion injury after ischemic stroke in a rodent model of type 2 diabetes.Microcirculation (New York, N.Y. : 1994) · 2011Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The severity of ischaemic heart disease is markedly enhanced in type 2 diabetes. We recently reported that complement activation exacerbates I/R injury in the type 2 diabetic heart. The purpose of this study was to isolate and examine MBL pathway activation following I/R injury in the diabetic heart. ZLC and ZDF rats underwent 30 minutes of left coronary artery occlusion followed by 120 minutes of reperfusion. Two different groups of ZDF rats were treated with either FUT-175, a broad complement inhibitor, or P2D5, a monoclonal antibody raised against rat MBL-A. ZDF rats treated with FUT175 and P2D5 had significantly decreased myocardial infarct size, C3 deposition and neutrophil accumulation compared with untreated ZDF controls. Taken together, these findings indicate that the MBL pathway plays a key role in the severity of complement-mediated I/R injury in the type 2 diabetic heart.
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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.