ArticlePloS one2017
Activation of complement factor B contributes to murine and human myocardial ischemia/reperfusion injury.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Activation of the C3a-C3aReceptor-axis is associated with endothelial dysfunction and glycocalyx damage in ST-elevation myocardial infarction.Basic research in cardiology · 2026Article
- Kidney-Lung Crosstalk in Acute Nephrologic Involvement: Mechanisms, Complement Activation, and Implications for Multiorgan Dysfunction.Life (Basel, Switzerland) · 2026Review
- A Comprehensive Review: Unraveling the Role of Inflammation in the Etiology of Heart Failure.Heart failure reviews · 2025Review
- Exosomal HSP90 induced by remote ischemic preconditioning alleviates myocardial ischemia/reperfusion injury by inhibiting complement activation and inflammation.BMC cardiovascular disorders · 2023Article
- Properdin inhibition ameliorates hepatic ischemia/reperfusion injury without interfering with liver regeneration in mice.Frontiers in immunology · 2023Article
- Contribution of animal models to the mechanistic understanding of Alternative Pathway and Amplification Loop (AP/AL)-driven Complement-mediated Diseases.Immunological reviews · 2023Review
- Intracellular Complement Component 3 Attenuated Ischemia-Reperfusion Injury in the Isolated Buffer-Perfused Mouse Heart and Is Associated With Improved Metabolic Homeostasis.Frontiers in immunology · 2022Article
- Increasing the efficacy and safety of a human complement inhibitor for treating post-transplant cardiac ischemia reperfusion injury by targeting to a graft-specific neoepitope.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2021Article
- Postconditioning attenuates myocardial ischemia-reperfusion injury by inhibiting complement activation and upregulation of miR-499.Experimental and therapeutic medicine · 2021Article
- Sterile inflammation in thoracic transplantation.Cellular and molecular life sciences : CMLS · 2021Review
- New targets of morphine postconditioning protection of the myocardium in ischemia/reperfusion injury: Involvement of HSP90/Akt and C5a/NF-κB.Open medicine (Warsaw, Poland) · 2021Article
- The Role of Complement in Myocardial Infarction Reperfusion Injury: An Underappreciated Therapeutic Target.Frontiers in cell and developmental biology · 2020Review
- Involvement of HSP90 in ischemic postconditioning-induced cardioprotection by inhibition of the complement system, JNK and inflammation.Acta cirurgica brasileira · 2020Article
- Complement activation by autoantigen recognition in the growth process of benign prostatic hyperplasia.Scientific reports · 2019Article
- Blocking Complement Factor B Activation Reduces Renal Injury and Inflammation in a Rat Brain Death Model.Frontiers in immunology · 2019Article
- Role of Inflammatory Cell Subtypes in Heart Failure.Journal of immunology research · 2019Review
- Anti-Inflammatory Effects of Resveratrol: Mechanistic Insights.International journal of molecular sciences · 2018Review
- The Alternative Complement System Mediates Cell Death in Retinal Ischemia Reperfusion Injury.Frontiers in molecular neuroscience · 2018Article
- Non-Invasive whole-body detection of complement activation using radionuclide imaging in a mouse model of myocardial ischaemia-reperfusion injury.Scientific reports · 2017Article
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Authors and funding
21 authors at 5 institutions in 2 countries.
Funding
Abstract
The pathophysiology of myocardial injury that results from cardiac ischemia and reperfusion (I/R) is incompletely understood. Experimental evidence from murine models indicates that innate immune mechanisms including complement activation via the classical and lectin pathways are crucial. Whether factor B (fB), a component of the alternative complement pathway required for amplification of complement cascade activation, participates in the pathophysiology of myocardial I/R injury has not been addressed. We induced regional myocardial I/R injury by transient coronary ligation in WT C57BL/6 mice, a manipulation that resulted in marked myocardial necrosis associated with activation of fB protein and myocardial deposition of C3 activation products. In contrast, in fB-/- mice, the same procedure resulted in significantly reduced myocardial necrosis (% ventricular tissue necrotic; fB-/- mice, 20 ± 4%; WT mice, 45 ± 3%; P < 0.05) and diminished deposition of C3 activation products in the myocardial tissue (fB-/- mice, 0 ± 0%; WT mice, 31 ± 6%; P<0.05). Reconstitution of fB-/- mice with WT serum followed by cardiac I/R restored the myocardial necrosis and activated C3 deposition in the myocardium. In translational human studies we measured levels of activated fB (Bb) in intracoronary blood samples obtained during cardio-pulmonary bypass surgery before and after aortic cross clamping (AXCL), during which global heart ischemia was induced. Intracoronary Bb increased immediately after AXCL, and the levels were directly correlated with peripheral blood levels of cardiac troponin I, an established biomarker of myocardial necrosis (Spearman coefficient = 0.465, P < 0.01). Taken together, our results support the conclusion that circulating fB is a crucial pathophysiological amplifier of I/R-induced, complement-dependent myocardial necrosis and identify fB as a potential therapeutic target for prevention of human myocardial I/R injury.
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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.