Evidence map›Paper›PMID 25126549›Full record

ReviewBioMed research international2014

Cell death and inflammatory bowel diseases: apoptosis, necrosis, and autophagy in the intestinal epithelium.

Tiago Nunes, Claudio Bernardazzi, Heitor S de Souza

Open access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

74 citing papers in PubMed, 167 citations in OpenAlex.

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  19. Toxins · 2023
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14 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

3 authors at 2 institutions in 2 countries.

Tiago NunesNutrition and Immunology Chair, ZIEL-Research Center for Nutrition and Food Sciences, Technical University of Munich, Weihenstephan, 85354 Freising, Germany.ORCID 0000-0003-2134-4171
Claudio BernardazziServiço de Gastroenterologia & Laboratório Multidisciplinar de Pesquisa, Hospital Universitario, Universidade Federal do Rio de Janeiro, Rua Professor Rodolpho Paulo Rocco 255, Ilha do Fundão, 21941-913 Rio de Janeiro, RJ, Brazil.ORCID 0000-0003-4774-902X
Heitor S de SouzaServiço de Gastroenterologia & Laboratório Multidisciplinar de Pesquisa, Hospital Universitario, Universidade Federal do Rio de Janeiro, Rua Professor Rodolpho Paulo Rocco 255, Ilha do Fundão, 21941-913 Rio de Janeiro, RJ, Brazil ; D'Or Institute for Research and Education (IDOR), Rua Diniz Cordeiro 30, Botafogo, 22281-100 Rio de Janeiro, RJ, Brazil.ORCID 0000-0002-3647-7324
Universidade Federal do Rio de Janeiro · BRTechnical University of Munich · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell death mechanisms have been associated with the development of inflammatory bowel diseases in humans and mice. Recent studies suggested that a complex crosstalk between autophagy/apoptosis, microbe sensing, and enhanced endoplasmic reticulum stress in the epithelium could play a critical role in these diseases. In addition, necroptosis, a relatively novel programmed necrosis-like pathway associated with TNF receptor activation, seems to be also present in the pathogenesis of Crohn's disease and in specific animal models for intestinal inflammation. This review attempts to cover new data related to cell death mechanisms and inflammatory bowel diseases.

Indexed as

AnimalsApoptosisAutophagyHumansInflammatory Bowel DiseasesIntestinal MucosaMiceNecrosisSignal Transduction

Identifiers

PMID25126549
PMCPMC4121991
OpenAlexW2022785083

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.