ReviewFrontiers in immunology2020
Inflammaging and Complement System: A Link Between Acute Kidney Injury and Chronic Graft Damage.
Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 61 papers, 2 of them syntheses that pooled it.
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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.
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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.
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Who cites it
61 citing papers in PubMed, 2 syntheses or guidelines pooled it, 85 citations in OpenAlex.
- Prediction models for infection after kidney transplantation: a systematic review.Frontiers in medicine · 2026Pooled it
- Pitfalls in complement analysis: A systematic literature review of assessing complement activation.Frontiers in immunology · 2022Pooled it
- Fibrinogen-like protein 2-complement C3 interaction exacerbates tubular inflammation in acute kidney injury by elevating complement C3a levels.Renal failure · 2026Article
- Immunosenescence and cancer predisposition in pediatric transplant recipients: An emerging paradigm.World journal of transplantation · 2026Review
- A comprehensive review on the role of PM2.5 in modulating transplant immunity and graft survival.Particle and fibre toxicology · 2026Review
- Targeting C1q signaling in fibro-adipogenic progenitors prevents regenerative fibrosis of aged muscle.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Discovery Pipeline for Acute Kidney Injury: Molecules, Mechanisms, Models, and Targets.Nephron · 2026Review
- Single-section multiplex spatial proteomics of immune microenvironments in kidney transplantation.Frontiers in immunology · 2026Article
- Complement in acute kidney injury: a convergent pathogenic pathway in multifactorial renal damage.Frontiers in immunology · 2026Review
- Inhibition of FXIIa attenuates kidney fibrosis in mice with unilateral ureteral obstruction.Cellular and molecular life sciences : CMLS · 2025Article
- Exogenous spexin aggravates renal ischemia reperfusion injury and triggers toxicity in healthy kidneys.Frontiers of medicine · 2025Article
- From acute kidney injury to chronic kidney disease in children: maladaptive repair and the need for long-term surveillance - a literature review.BMC nephrology · 2025Review
- Molecular mechanisms and therapeutic interventions in acute kidney injury: a literature review.BMC nephrology · 2025Review
- mTOR Inhibition limits LPS induced acute kidney injury and ameliorates hallmarks of cellular senescence.Scientific reports · 2025Article
- Targeting senescence to prevent diabetic kidney disease: Exploring molecular mechanisms and potential therapeutic targets for disease management.Diabetic medicine : a journal of the British Diabetic Association · 2025Review
- Vascular inflammaging: Endothelial CEACAM1 expression is upregulated by TNF-α via independent activation of NF-κB and β-catenin signaling.Aging cell · 2025Article
- Exploring Potential Complement Modulation Strategies for Ischemia-Reperfusion Injury in Kidney Transplantation.Antioxidants (Basel, Switzerland) · 2025Review
- Effect of probiotics on the incidence of acute kidney injury in patients with severe pneumonia.Frontiers in medicine · 2025Article
- Role of NHERF1 in MicroRNA Landscape Changes in Aging Mouse Kidneys.Biomolecules · 2024Article
- 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
1 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aberrant activation of complement system in several kidney diseases suggests that this pillar of innate immunity has a critical role in the pathophysiology of renal damage of different etiologies. A growing body of experimental evidence indicates that complement activation contributes to the pathogenesis of acute kidney injury (AKI) such as delayed graft function (DGF) in transplant patients. AKI is characterized by the rapid loss of the kidney's excretory function and is a complex syndrome currently lacking a specific medical treatment to arrest or attenuate progression in chronic kidney disease (CKD). Recent evidence suggests that independently from the initial trigger (i.e., sepsis or ischemia/reperfusions injury), an episode of AKI is strongly associated with an increased risk of subsequent CKD. The AKI-to-CKD transition may involve a wide range of mechanisms including scar-forming myofibroblasts generated from different sources, microvascular rarefaction, mitochondrial dysfunction, or cell cycle arrest by the involvement of epigenetic, gene, and protein alterations leading to common final signaling pathways [i.e., transforming growth factor beta (TGF-β), p16
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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.