Evidence map›Paper›PMID 21562469›Full record

ReviewKidney international2011

Apoptosis and acute kidney injury.

Andrea Havasi, Steven C Borkan

Open access · bronzeAbstract readReview
In one paragraph

Review in Kidney international, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 351 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
351citing papers in PubMed, 1 pooled it
16.6field-weighted citation impact, top 1% 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.

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

351 citing papers in PubMed, 1 synthesis or guideline pooled it, 629 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
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  5. Article
  6. Review
  7. Article
  8. Article
  9. Apoptotic Bodies in Kidney Disease: Orchestrators of Inflammation, Fibrosis, and Repair.Journal of the American Society of Nephrology : JASN · 2026
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
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291 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Andrea HavasiRenal Section, Department of Medicine, Boston University, Boston, Massachusetts 02118, USA.
Steven C Borkan
Boston University · US

Funding

CYTOPROTECTIVE ROLE OF HSP72 IN RENAL CELL INJURYR01DK053387 · NIDDK · BOSTON MEDICAL CENTER · PI BORKAN, STEVEN C. · 1999 to 2016
$5.1M
Proteinuria causes progressive kidney disease by impairing autophagyK08DK090143 · NIDDK · BOSTON MEDICAL CENTER · PI HAVASI, ANDREA · 2011 to 2015
$746k
NIDDK NIH HHS DK-53387NIDDK NIH HHS K08 DK090143NIDDK NIH HHS R01 DK053387
6 · The paper itself

Abstract

Improved mechanistic understanding of renal cell death in acute kidney injury (AKI) has generated new therapeutic targets. Clearly, the classic lesion of acute tubular necrosis is not adequate to describe the consequences of renal ischemia, nephrotoxin exposure, or sepsis on glomerular filtration rate. Experimental evidence supports a pathogenic role for apoptosis in AKI. Interestingly, proximal tubule epithelial cells are highly susceptible to apoptosis, and injury at this site contributes to organ failure. During apoptosis, well-orchestrated events converge at the mitochondrion, the organelle that integrates life and death signals generated by the BCL2 (B-cell lymphoma 2) protein family. Death requires the 'perfect storm' for outer mitochondrial membrane injury to release its cellular 'executioners'. The complexity of this process affords new targets for effective interventions, both before and after renal insults. Inhibiting apoptosis appears to be critical, because circulating factors released by the injured kidney induce apoptosis and inflammation in distant organs including the heart, lung, liver, and brain, potentially contributing to the high morbidity and mortality associated with AKI. Manipulation of known stress kinases upstream of mitochondrial injury, induction of endogenous, anti-apoptotic proteins, and improved understanding of the timing and consequences of renal cell apoptosis will inevitably improve the outcome of human AKI.

Indexed as

ApoptosisAcute Kidney InjuryAnimalsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansIschemiaKidneyModels, BiologicalProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2Shock, SepticSignal TransductionStress, PhysiologicalGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2

Identifiers

PMID21562469
PMCPMC4625984
OpenAlexW2067463198

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.