ReviewFibrogenesis & tissue repair2014
The role of complement in the pathogenesis of renal ischemia-reperfusion injury and fibrosis.
Review in Fibrogenesis & tissue repair, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
60 citing papers in PubMed, 2 syntheses or guidelines pooled it, 100 citations in OpenAlex.
- Effects and Mechanisms of Fisetin against Ischemia-reperfusion Injuries: A Systematic Review.Current pharmaceutical biotechnology · 2024Pooled it
- The Effect of Hypothermic Machine Perfusion to Ameliorate Ischemia-Reperfusion Injury in Donor Organs.Frontiers in immunology · 2022Pooled it
- Effect of complement 3/5 knockout on renal proteomics landscape after ischemia and reperfusion injury in rats.Physiological reports · 2026Article
- Nanoadjuvant-integrated organic biomaterials for immune engineering: Mechanisms, design strategies, and translational applications.Materials today. Bio · 2026Review
- Urinary CFHR2 as a Biomarker for Early Diagnosis and Disease Progression Prediction in Diabetic Kidney Disease.Current molecular medicine · 2026Article
- Cellular and Molecular Aspects of Chronic Rejection.Results and problems in cell differentiation · 2026Review
- Critical role of complement in antibody mediated rejection in kidney transplantation.World journal of transplantation · 2025Review
- Complement C3 deficiency enhances renal leptospiral load and inflammation while impairing T cell differentiation during chronicInfection and immunity · 2025Article
- Complement C3 in panvascular disease: a central integrator of immune signaling and vascular remodeling.Clinical science (London, England : 1979) · 2025Review
- Review
- Article
- Kidney Injury Following Cardiac Surgery: A Review of Our Current Understanding.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2025Review
- Leucine-rich alpha-2-glycoprotein 1 deficiency suppresses ischemia-reperfusion injury-induced renal fibrosis.Scientific reports · 2025Article
- Macrophage-Induced Pro-Fibrotic Gene Expression in Tubular Cells after Ischemia/Reperfusion Is Paralleled but Not Directly Mediated by C5a/C5aR1 Signaling.Life (Basel, Switzerland) · 2024Article
- Neutrophil extracellular traps and citrullinated fibrinogen contribute to injury in a porcine model of limb ischemia and reperfusion.Frontiers in immunology · 2024Article
- Therapeutic Potential of Targeting Complement C5a Receptors in Diabetic Kidney Disease.International journal of molecular sciences · 2023Review
- Proteomics reveals specific biological changes induced by the normothermic machine perfusion of donor kidneys with a significant up-regulation of Latexin.Scientific reports · 2023Article
- Complement C3 mediates podocyte injury through TLR4/NFΚB-P65 signaling during ischemia-reperfusion acute kidney injury and post-injury fibrosis.European journal of medical research · 2023Article
- How to Best Protect Kidneys for Transplantation-Mechanistic Target.Journal of clinical medicine · 2023Review
- Diclofenac Disrupts the Circadian Clock and through Complex Cross-Talks Aggravates Immune-Mediated Liver Injury-A Repeated Dose Study in Minipigs for 28 Days.International journal of molecular sciences · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The complement system is a major component of innate immunity and has been commonly identified as a central element in host defense, clearance of immune complexes, and tissue homeostasis. After ischemia-reperfusion injury (IRI), the complement system is activated by endogenous ligands that trigger proteolytic cleavage of complement components via the classical, lectin and/or alternative pathway. The result is the formation of terminal complement components C3a, C5a, and the membrane attack complex (C5b-9 or MAC), all of which play pivotal roles in the amplification of the inflammatory response, chemotaxis, neutrophil/monocyte recruitment and activation, and direct tubular cell injury. However, recent evidence suggests that complement activity transcends innate host defense and there is increasing data suggesting complement as a regulator in processes such as allo-immunity, stem cell differentiation, tissue repair, and progression to fibrosis. In this review, we discuss recent advances addressing the role of complement as a regulator of IRI and renal fibrosis after organ donation for transplantation. We will also briefly discuss currently approved therapies that target complement activity in kidney ischemia-reperfusion and transplantation.
Identifiers
What OpenQuestion holds
Registered trials
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.