Evidence map›Paper›PMID 21197658›Full record

ReviewWiley interdisciplinary reviews. Systems biology and medicine

Ischemic kidney injury and mechanisms of tissue repair.

Marwa El Sabbahy, Vishal S Vaidya

Abstract readReview
In one paragraph

Review in Wiley interdisciplinary reviews. Systems biology and medicine. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
–field-weighted citation impact
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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

41 citing papers in PubMed.

  1. Article
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  4. Review
  5. Review
  6. Article
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  8. Article
  9. Article
  10. Review
  11. Article
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  14. The analysis of a time-course transcriptome profile by systems biology approaches reveals key molecular processes in acute kidney injury.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2019
    Article
  15. Review
  16. Early life stress induces immune priming in kidneys of adult male rats.American journal of physiology. Renal physiology · 2018
    Article
  17. Article
  18. Mitochondrial energetics in the kidney.Nature reviews. Nephrology · 2017
    Review
  19. Article
  20. Review
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

2 authors.

Marwa El SabbahyLaboratory of Kidney Toxicology and Regeneration, Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Harvard Institutes of Medicine, Boston, MA, USA.
Vishal S Vaidya

Funding

HARVARD CLINICAL AND TRANSLATIONAL SCIENCE CENTER (UL1)UL1RR025758 · NCRR · HARVARD MEDICAL SCHOOL · PI NADLER, LEE MARSHALL · 2008 to 2011
$91.4M
Technology and Endothelial Biology of Kidney Injury Molecule-1R00ES016723 · NIEHS · BRIGHAM AND WOMEN'S HOSPITAL · PI VAIDYA, VISHAL S. · 2008 to 2010
$983k
Technology and Endothelial Biology of Kidney Injury Molecule-1K99ES016723 · NIEHS · BRIGHAM AND WOMEN'S HOSPITAL · PI VAIDYA, VISHAL S. · 2007 to 2007
$90k
NCRR NIH HHS 1 UL1 RR 025758-02NCRR NIH HHS UL1 RR025758NIEHS NIH HHS ES016723NIEHS NIH HHS K99 ES016723NIEHS NIH HHS R00 ES016723
6 · The paper itself

Abstract

Acute kidney injury (AKI) may result from ischemia or by the use of nephrotoxic agents. The incidence of AKI is variable, depends on comorbidities, and ranges from 5 to 35% in all hospitalized patients. The mechanisms of kidney injury exist within a large network of signaling pathways driven by interplay of inflammatory cytokines/chemokines, reactive oxygen species (ROS), and apoptotic factors. The effects and progression of injury overlap extensively with the remarkable ability of the kidney to repair itself both by intrinsic and extrinsic mechanisms that involve specific cell receptors/ligands as well as possible paracrine influences. The fact that kidney injury is usually part of a generalized comorbid condition makes it all the more challenging in terms of assessment of severity. In this review, we attempt to analyze the mechanisms of ischemic injury and repair in acute and chronic kidney disease from the perspectives of both preclinical and human studies.

Indexed as

Wound HealingAcute Kidney InjuryApoptosisHumansImmunologic FactorsInflammation MediatorsIschemiaOxidative StressReactive Oxygen SpeciesSignal TransductionStem CellsImmunologic FactorsInflammation MediatorsReactive Oxygen Species

Identifiers

PMID21197658
PMCPMC3087860

What OpenQuestion holds

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Registered trials

None linked

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.