Evidence map›Paper›PMID 31340541›Full record

ReviewInternational journal of molecular sciences2019

Cell Death in the Kidney.

Giovanna Priante, Lisa Gianesello, Monica Ceol, Dorella Del Prete, Franca Anglani

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed, 1 pooled it
12.4field-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

109 citing papers in PubMed, 1 synthesis or guideline pooled it, 169 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Apoptotic Bodies in Kidney Disease: Orchestrators of Inflammation, Fibrosis, and Repair.Journal of the American Society of Nephrology : JASN · 2026
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Nephrotoxic acute kidney injury induced byThe journal of venomous animals and toxins including tropical diseases · 2026
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

49 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

5 authors at 1 institution in 1 country.

Giovanna PrianteKidney Histomorphology and Molecular Biology Laboratory, Clinical Nephrology, Department of Medicine - DIMED, University of Padua, via Giustiniani 2, 35128 Padova, Italy. giovanna.priante@unipd.it.ORCID 0000-0002-1870-4466
Lisa GianeselloKidney Histomorphology and Molecular Biology Laboratory, Clinical Nephrology, Department of Medicine - DIMED, University of Padua, via Giustiniani 2, 35128 Padova, Italy.ORCID 0000-0001-9327-397X
Monica CeolKidney Histomorphology and Molecular Biology Laboratory, Clinical Nephrology, Department of Medicine - DIMED, University of Padua, via Giustiniani 2, 35128 Padova, Italy.
Dorella Del PreteKidney Histomorphology and Molecular Biology Laboratory, Clinical Nephrology, Department of Medicine - DIMED, University of Padua, via Giustiniani 2, 35128 Padova, Italy.
Franca AnglaniKidney Histomorphology and Molecular Biology Laboratory, Clinical Nephrology, Department of Medicine - DIMED, University of Padua, via Giustiniani 2, 35128 Padova, Italy.
University of Padua · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apoptotic cell death is usually a response to the cell's microenvironment. In the kidney, apoptosis contributes to parenchymal cell loss in the course of acute and chronic renal injury, but does not trigger an inflammatory response. What distinguishes necrosis from apoptosis is the rupture of the plasma membrane, so necrotic cell death is accompanied by the release of unprocessed intracellular content, including cellular organelles, which are highly immunogenic proteins. The relative contribution of apoptosis and necrosis to injury varies, depending on the severity of the insult. Regulated cell death may result from immunologically silent apoptosis or from immunogenic necrosis. Recent advances have enhanced the most revolutionary concept of regulated necrosis. Several modalities of regulated necrosis have been described, such as necroptosis, ferroptosis, pyroptosis, and mitochondrial permeability transition-dependent regulated necrosis. We review the different modalities of apoptosis, necrosis, and regulated necrosis in kidney injury, focusing particularly on evidence implicating cell death in ectopic renal calcification. We also review the evidence for the role of cell death in kidney injury, which may pave the way for new therapeutic opportunities.

Indexed as

Acute Kidney InjuryAnimalsApoptosisApoptosis Regulatory ProteinsCalcinosisEpithelial CellsFerroptosisGene Expression RegulationHumansImmunogenic Cell DeathKidneyMitochondrial Transmembrane Permeability-Driven NecrosisNecroptosisNecrosisProtective AgentsPyroptosisApoptosis Regulatory ProteinsProtective Agentsapoptosisglomerular injurykidney injurynecrosisregulated necrosistubular injury

Identifiers

PMID31340541
PMCPMC6679187
OpenAlexW2963986056

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.