Evidence map›Paper›PMID 36959481›Full record

ReviewNature reviews. Nephrology2023

Regulated cell death pathways in kidney disease.

Ana B Sanz, Maria Dolores Sanchez-Niño, Adrian M Ramos, Alberto Ortiz

Open access · bronzeAbstract readReview
In one paragraph

Review in Nature reviews. Nephrology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 253 papers.

0numbers the graph read from it
0cells of the map it votes in
253citing papers in PubMed
63.0field-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

253 citing papers in PubMed, 318 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. The gasdermin family: from pyroptosis mechanisms to therapeutic targets.Signal transduction and targeted therapy · 2026
    Review
  11. Article
  12. Ferroptosis in kidney disease.Nature reviews. Nephrology · 2026
    Review
  13. A mitochondria-targeted HRedox biology · 2026
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. TRIM21 inhibition alleviates acute kidney injury by promoting INTS3-associated DNA damage repair.Apoptosis : an international journal on programmed cell death · 2026
    Article
  19. Magnesium Attenuates Renal Senescence and Fibrosis With Reduced DNA Damage Response and H3K4me3 Enrichment at the p16FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  20. Review

193 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

4 authors at 2 institutions in 1 country.

Ana B SanzDepartment of Nephrology and Hypertension, IIS-Fundacion Jimenez Diaz UAM, Madrid, Spain.
Maria Dolores Sanchez-NiñoDepartment of Nephrology and Hypertension, IIS-Fundacion Jimenez Diaz UAM, Madrid, Spain.
Adrian M RamosDepartment of Nephrology and Hypertension, IIS-Fundacion Jimenez Diaz UAM, Madrid, Spain.
Alberto OrtizDepartment of Nephrology and Hypertension, IIS-Fundacion Jimenez Diaz UAM, Madrid, Spain. aortiz@fjd.es.ORCID 0000-0002-9805-9523
Hospital Universitario Fundación Jiménez Díaz · ESUniversidad de Cádiz · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disorders of cell number that result from an imbalance between the death of parenchymal cells and the proliferation or recruitment of maladaptive cells contributes to the pathogenesis of kidney disease. Acute kidney injury can result from an acute loss of kidney epithelial cells. In chronic kidney disease, loss of kidney epithelial cells leads to glomerulosclerosis and tubular atrophy, whereas interstitial inflammation and fibrosis result from an excess of leukocytes and myofibroblasts. Other conditions, such as acquired cystic disease and kidney cancer, are characterized by excess numbers of cyst wall and malignant cells, respectively. Cell death modalities act to clear unwanted cells, but disproportionate responses can contribute to the detrimental loss of kidney cells. Indeed, pathways of regulated cell death - including apoptosis and necrosis - have emerged as central events in the pathogenesis of various kidney diseases that may be amenable to therapeutic intervention. Modes of regulated necrosis, such as ferroptosis, necroptosis and pyroptosis may cause kidney injury directly or through the recruitment of immune cells and stimulation of inflammatory responses. Importantly, multiple layers of interconnections exist between different modalities of regulated cell death, including shared triggers, molecular components and protective mechanisms.

Indexed as

Acute Kidney InjuryFerroptosisApoptosisHumansKidneyNecrosis

Identifiers

PMID36959481
PMCPMC10035496
OpenAlexW4360612283

What Socratic 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 Socratic graph.