ArticlePloS one2013
C1 esterase inhibitor reduces lower extremity ischemia/reperfusion injury and associated lung damage.
Article in PloS one, 2013. 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, 35 citations in OpenAlex.
- Therapeutic Potential of C1-Inhibitor in Vascular Diseases and Beyond.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Advances in the treatment of lower-extremity ischemia-reperfusion injury.Frontiers in pharmacology · 2025Review
- Mitochondrial transplantation reduces lower limb ischemia-reperfusion injury by increasing skeletal muscle energy and adipocyte browning.Molecular therapy. Methods & clinical development · 2023Article
- DNase I and Sivelestat Ameliorate Experimental Hindlimb Ischemia-Reperfusion Injury by Eliminating Neutrophil Extracellular Traps.Journal of inflammation research · 2023Article
- Asthma and Post-Asthmatic Fibrosis: A Search for New Promising Molecular Markers of Transition from Acute Inflammation to Pulmonary Fibrosis.Biomedicines · 2022Article
- Improving the ischemia-reperfusion injury in vascularized composite allotransplantation: Clinical experience and experimental implications.Frontiers in immunology · 2022Review
- Quantitative iTRAQ LC-MS/MS reveals muscular proteome profiles of deep pressure ulcers.Bioscience reports · 2020Article
- Effect of complement C1-esterase inhibitor on brain edema and inflammation after mild traumatic brain injury in an animal model.Clinical and experimental emergency medicine · 2020Article
- SERPINs-From Trap to Treatment.Frontiers in medicine · 2019Review
- 3D artificial round section micro-vessels to investigate endothelial cells under physiological flow conditions.Scientific reports · 2018Article
- Potential Roles for C1 Inhibitor in Transplantation.Transplantation · 2016Review
- Contribution of the anaphylatoxin receptors, C3aR and C5aR, to the pathogenesis of pulmonary fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Alternative Interventions to Prevent Oxidative Damage following Ischemia/Reperfusion.Oxidative medicine and cellular longevity · 2016Review
- Vasculitides and the Complement System: a Comprehensive Review.Clinical reviews in allergy & immunology · 2015Review
- Functional expression of bradykinin B1 and B2 receptors in neonatal rat trigeminal ganglion neurons.Frontiers in cellular neuroscience · 2015Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
backgroundIschemia/reperfusion injury of lower extremities and associated lung damage may result from thrombotic occlusion, embolism, trauma, or surgical intervention with prolonged ischemia and subsequent restoration of blood flow. This clinical entity is characterized by high morbidity and mortality. Deprivation of blood supply leads to molecular and structural changes in the affected tissue. Upon reperfusion inflammatory cascades are activated causing tissue injury. We therefore tested preoperative treatment for prevention of reperfusion injury by using C1 esterase inhibitor (C1 INH). METHODS AND
findingsWistar rats systemically pretreated with C1 INH (n = 6), APT070 (a membrane-targeted myristoylated peptidyl construct derived from human complement receptor 1, n = 4), vehicle (n = 7), or NaCl (n = 8) were subjected to 3h hind limb ischemia and 24h reperfusion. The femoral artery was clamped and a tourniquet placed under maintenance of a venous return. C1 INH treated rats showed significantly less edema in muscle (P<0.001) and lung and improved muscle viability (P<0.001) compared to controls and APT070. C1 INH prevented up-regulation of bradykinin receptor b1 (P<0.05) and VE-cadherin (P<0.01), reduced apoptosis (P<0.001) and fibrin deposition (P<0.01) and decreased plasma levels of pro-inflammatory cytokines, whereas deposition of complement components was not significantly reduced in the reperfused muscle.
conclusionsC1 INH reduced edema formation locally in reperfused muscle as well as in lung, and improved muscle viability. C1 INH did not primarily act via inhibition of the complement system, but via the kinin and coagulation cascade. APT070 did not show beneficial effects in this model, despite potent inhibition of complement activation. Taken together, C1 INH might be a promising therapy to reduce peripheral ischemia/reperfusion injury and distant lung damage in complex and prolonged surgical interventions requiring tourniquet application.
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