Evidence map›Paper›PMID 26413280›Full record

ReviewClinical kidney journal2015

Pathophysiological role of different tubular epithelial cell death modes in acute kidney injury.

Sandra M Sancho-Martínez, José M López-Novoa, Francisco J López-Hernández

Open access · goldAbstract readReview
In one paragraph

Review in Clinical kidney journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
7.2field-weighted citation impact, top 2% 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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 126 citations in OpenAlex.

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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

3 authors at 2 institutions in 1 country.

Sandra M Sancho-MartínezDepartamento de Fisiología y Farmacología , Universidad de Salamanca , Salamanca , Spain ; Instituto de Investigación Biomédica de Salamanca (IBSAL) , Salamanca , Spain ; Instituto Reina Sofía de Investigación Nefrológica, Fundación Iñigo Álvarez de Toledo , Madrid , Spain.
José M López-NovoaDepartamento de Fisiología y Farmacología , Universidad de Salamanca , Salamanca , Spain ; Instituto de Investigación Biomédica de Salamanca (IBSAL) , Salamanca , Spain ; Instituto Reina Sofía de Investigación Nefrológica, Fundación Iñigo Álvarez de Toledo , Madrid , Spain ; Critical Care Biomedical Research Group (BioCritic) , Valladolid , Spain.
Francisco J López-HernándezDepartamento de Fisiología y Farmacología , Universidad de Salamanca , Salamanca , Spain ; Instituto de Investigación Biomédica de Salamanca (IBSAL) , Salamanca , Spain ; Instituto Reina Sofía de Investigación Nefrológica, Fundación Iñigo Álvarez de Toledo , Madrid , Spain ; Critical Care Biomedical Research Group (BioCritic) , Valladolid , Spain ; Instituto de Estudios de Ciencias de la Salud de Castilla y León (IESCYL) , Salamanca , Spain.
Fundación Renal · ESInstituto de Estudios de Ciencias de la Salud de Castilla y León · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The histological substrate of many forms of intrinsic acute kidney injury (AKI) has been classically attributed to tubular necrosis. However, more recent studies indicate that necrosis is not the main form of cell death in AKI and that other forms such as apoptosis, regulated necrosis (i.e. necroptosis and parthanatos), autophagic cell death and mitotic catastrophe, also participate in AKI and that their contribution depends on the cause and stage of AKI. Herein, we briefly summarize the main characteristics of the major types of cell death and we also critically review the existing evidence on the occurrence of different types of cell death reported in the most common experimental models of AKI and human specimens. We also discuss the pathophysiological mechanisms linking tubule epithelial cell death with reduced glomerular filtration, azotaemia and hydroelectrolytic imbalance. For instance, special relevance is given to the analysis of the inflammatory component of some forms of cell death over that of others, as an important and differential pathophysiological determinant. Finally, known molecular mechanisms and signalling pathways involved in each cell death type pose appropriate targets to specifically prevent or reverse AKI, provided that further knowledge of their participation and repercussion in each AKI syndrome is progressively increased in the near future.

Indexed as

apoptosisautophagyferroptosisnecroptosispathophysiology

Identifiers

PMID26413280
PMCPMC4581387
OpenAlexW2261452917

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.