Evidence map›Paper›PMID 12067448›Full record

ReviewJournal of cellular and molecular medicine

Contribution of apoptotic cell death to renal injury.

A Ortiz, C Lorz, P Justo, M P Catalán, J Egido

Abstract readReview
In one paragraph

Review in Journal of cellular and molecular medicine. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Tumor necrosis factor-α: regulation of renal function and blood pressure.American journal of physiology. Renal physiology · 2013
    Review
  12. Article
  13. Decoy receptor 3, a novel inflammatory marker, and mortality in hemodialysis patients.Clinical journal of the American Society of Nephrology : CJASN · 2012
    Article
  14. Article
  15. Article
  16. Article
  17. tPA protects renal interstitial fibroblasts and myofibroblasts from apoptosis.Journal of the American Society of Nephrology : JASN · 2008
    Article
  18. Article
  19. Genetic deletion of p66(Shc) adaptor protein prevents hyperglycemia-induced endothelial dysfunction and oxidative stress.Proceedings of the National Academy of Sciences of the United States of America · 2007
    Article
  20. Article
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

5 authors.

A OrtizUnidad de Dialisis, Fundacion Jimenez Diaz, Av Reyes Catolicos 2, 28040 Madrid, Spain. aortiz@fjd.es
C Lorz
P Justo
M P Catalán
J Egido

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell number abnormalities are frequent in renal diseases, and range from the hypercellularity of postinfectious glomerulonephritis to the cell depletion of chronic renal atrophy. Recent research has shown that apoptosis and its regulatory mechanisms contribute to cell number regulation in the kidney. The role of apoptosis ranges from induction to repair and progression of renal injury. Death ligands and receptors, such as TNF and FasL, proapoptotic and antiapoptotic Bcl-2 family members and caspases have all been shown to participate in apoptosis regulation in the course of renal injury. These proteins represent potential therapeutic targets, which should be further explored.

Indexed as

ApoptosisAnimalsCaspasesCytokinesHumansKidneyKidney DiseasesMitochondriaReceptors, Tumor Necrosis FactorCaspasesCytokinesReceptors, Tumor Necrosis Factor

Identifiers

PMID12067448
PMCPMC6737749

What OpenQuestion holds

Textmetadata
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.