Evidence map›Paper›PMID 22797180›Full record

ArticleJournal of the American Society of Nephrology : JASN2012

C3a and C5a promote renal ischemia-reperfusion injury.

Qi Peng, Ke Li, Lesley A Smyth, Guolan Xing, Naiyin Wang, Lucy Meader, Bao Lu, Steven H Sacks, Wuding Zhou

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03791476 (A Phase I/II,Single Center,Randomized,Double-Blind,Placebo-Controlled Study to Evaluate the Feasibility of Using Human Recombinant C1 Inhibitor), which is not on this map. Cited by 127 papers.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed
5.7field-weighted citation impact, top 3% of its field
1 · What the graph read from 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.

2 · The registry

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.

NCT03791476 phase1unknown statusnot on this mapstarted 2019, after this paper: background citation

A Phase I/II,Single Center,Randomized,Double-Blind,Placebo-Controlled Study to Evaluate the Feasibility of Using Human Recombinant C1 Inhibitor(RUCONEST®) as a Therapeutic Strategy to Reduce the Incidence of Delayed Graft Function in Recipients of Kidneys From Donation After Cardio-Circulatory Death

TypeinterventionalSponsorUniversity of Wisconsin, MadisonRan2019 to 2022Enrolled20ConditionsKidney FailureArmsrhC1INH, Saline Solution
3 · Its place in the literature

Who cites it

127 citing papers in PubMed, 211 citations in OpenAlex.

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  19. Role of local complement activation in kidney fibrosis and repair.The Journal of clinical investigation · 2025
    Review
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67 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 3 countries.

Qi PengMRC Centre for Transplantation, King's College London, London SE1 9RT, United Kingdom.
Ke Li
Lesley A Smyth
Guolan Xing
Naiyin Wang
Lucy Meader
Bao Lu
Steven H Sacks
Wuding Zhou
Medical Research Council · GBKing's College London · GBHarvard University · US

Funding

Medical Research Council G0600892Medical Research Council G0601202Medical Research Council G1001141Medical Research Council MR/J006742/1
6 · The paper itself

Abstract

Renal ischemia reperfusion injury triggers complement activation, but whether and how the small proinflammatory fragments C3a and C5a contribute to the pathogenesis of this injury remains to be elucidated. Using C3aR-, C5aR-, or C3aR/C5aR-deficient mice and models of renal ischemia-reperfusion injury, we found that deficiency of either or both of these receptors protected mice from injury, but the C3aR/C5aR- and C5aR-deficient mice were most protected. Protection from injury was associated with less cellular infiltration and lower mRNA levels of kidney injury molecule-1, proinflammatory mediators, and adhesion molecules in postischemic kidneys. Furthermore, chimera studies showed that the absence of C3aR and C5aR on renal tubular epithelial cells or circulating leukocytes attenuated renal ischemia-reperfusion injury. In vitro, C3a and C5a stimulation induced inflammatory mediators from both renal tubular epithelial cells and macrophages after hypoxia/reoxygenation. In conclusion, although both C3a and C5a contribute to renal ischemia-reperfusion injury, the pathogenic role of C5a in this injury predominates. These data also suggest that expression of C3aR and C5aR on both renal and circulating leukocytes contributes to the pathogenesis of renal ischemia-reperfusion injury.

Indexed as

AnimalsComplement C3aComplement C5aCytokinesFemaleHepatitis A Virus Cellular Receptor 1KidneyLeukocytesMaleMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutModels, AnimalRegional Blood FlowReperfusion InjuryComplement C3aComplement C5aCytokinesHavcr1 protein, mouseHepatitis A Virus Cellular Receptor 1Membrane Proteins

Identifiers

PMID22797180
PMCPMC3431410
OpenAlexW2155807513

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.