Evidence map›Paper›PMID 38077379›Full record

ReviewFrontiers in immunology2023

Regulated necrosis role in inflammation and repair in acute kidney injury.

Juan Guerrero-Mauvecin, Natalia Villar-Gómez, Sandra Rayego-Mateos, Adrian M Ramos, Marta Ruiz-Ortega, Alberto Ortiz, Ana B Sanz

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

34 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  7. Regulated cell death: a multidimensional regulatory network in the pathogenesis of renal fibrosis.Apoptosis : an international journal on programmed cell death · 2026
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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

7 authors at 2 institutions in 1 country.

Juan Guerrero-MauvecinLaboratorio de Nefrología Experimental, Instituto de Investigación Sanitaria-Fundación Jimenez Diaz (IIS-FJD), Universidad Autonoma de Madrid, Madrid, Spain.
Natalia Villar-GómezLaboratorio de Nefrología Experimental, Instituto de Investigación Sanitaria-Fundación Jimenez Diaz (IIS-FJD), Universidad Autonoma de Madrid, Madrid, Spain.
Sandra Rayego-MateosRedes de Investigación Cooperativa Orientadas a Resultados en Salud (RICORS2040), Madrid, Spain.
Adrian M RamosLaboratorio de Nefrología Experimental, Instituto de Investigación Sanitaria-Fundación Jimenez Diaz (IIS-FJD), Universidad Autonoma de Madrid, Madrid, Spain.
Marta Ruiz-OrtegaRedes de Investigación Cooperativa Orientadas a Resultados en Salud (RICORS2040), Madrid, Spain.
Alberto OrtizLaboratorio de Nefrología Experimental, Instituto de Investigación Sanitaria-Fundación Jimenez Diaz (IIS-FJD), Universidad Autonoma de Madrid, Madrid, Spain.
Ana B SanzLaboratorio de Nefrología Experimental, Instituto de Investigación Sanitaria-Fundación Jimenez Diaz (IIS-FJD), Universidad Autonoma de Madrid, Madrid, Spain.
Hospital Universitario Fundación Jiménez Díaz · ESUniversidad Autónoma de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute kidney injury (AKI) frequently occurs in patients with chronic kidney disease (CKD) and in turn, may cause or accelerate CKD. Therapeutic options in AKI are limited and mostly relate to replacement of kidney function until the kidneys recover spontaneously. Furthermore, there is no treatment that prevents the AKI-to-CKD transition. Regulated necrosis has recently emerged as key player in kidney injury. Specifically, there is functional evidence for a role of necroptosis, ferroptosis or pyroptosis in AKI and the AKI-to-CKD progression. Regulated necrosis may be proinflammatory and immunogenic, triggering subsequent waves of regulated necrosis. In a paradigmatic murine nephrotoxic AKI model, a first wave of ferroptosis was followed by recruitment of inflammatory cytokines such as TWEAK that, in turn, triggered a secondary wave of necroptosis which led to persistent kidney injury and decreased kidney function. A correct understanding of the specific forms of regulated necrosis, their timing and intracellular molecular pathways may help design novel therapeutic strategies to prevent or treat AKI at different stages of the condition, thus improving patient survival and the AKI-to-CKD transition. We now review key regulated necrosis pathways and their role in AKI and the AKI-to-CKD transition both at the time of the initial insult and during the repair phase following AKI.

Indexed as

Acute Kidney InjuryRenal Insufficiency, ChronicAnimalsApoptosisHumansInflammationMiceNecrosisacute kidney injurycell deathchronic kidney diseasefibrosisinflammationtissue repair

Identifiers

PMID38077379
PMCPMC10704359
OpenAlexW4388977062

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.