Evidence map›Paper›PMID 35408838›Full record

ReviewInternational journal of molecular sciences2022

Dysbiosis in Inflammatory Bowel Disease: Pathogenic Role and Potential Therapeutic Targets.

Patricia Teixeira Santana, Siane Lopes Bittencourt Rosas, Beatriz Elias Ribeiro, Ygor Marinho, Heitor S P de Souza

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 201 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
201citing papers in PubMed, 6 pooled it
51.2field-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

201 citing papers in PubMed, 6 syntheses or guidelines pooled it, 291 citations in OpenAlex.

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141 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.

Patricia Teixeira SantanaDepartment of Clinical Medicine, Federal University of Rio de Janeiro, Rio de Janeiro 21941-913, RJ, Brazil.ORCID 0000-0001-7888-5249
Siane Lopes Bittencourt RosasDepartment of Clinical Medicine, Federal University of Rio de Janeiro, Rio de Janeiro 21941-913, RJ, Brazil.
Beatriz Elias RibeiroDepartment of Clinical Medicine, Federal University of Rio de Janeiro, Rio de Janeiro 21941-913, RJ, Brazil.
Ygor MarinhoDepartment of Clinical Medicine, Federal University of Rio de Janeiro, Rio de Janeiro 21941-913, RJ, Brazil.
Heitor S P de SouzaDepartment of Clinical Medicine, Federal University of Rio de Janeiro, Rio de Janeiro 21941-913, RJ, Brazil.ORCID 0000-0002-3647-7324
Universidade Federal do Rio de Janeiro · BR

Funding

Coordenação de Aperfeicoamento de Pessoal de Nível Superior Finance Code 001Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro E26/202.781/2017Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro E26/210.886/2014National Council for Scientific and Technological Development 306634/2019-8
6 · The paper itself

Abstract

Microbe-host communication is essential to maintain vital functions of a healthy host, and its disruption has been associated with several diseases, including Crohn's disease and ulcerative colitis, the two major forms of inflammatory bowel disease (IBD). Although individual members of the intestinal microbiota have been associated with experimental IBD, identifying microorganisms that affect disease susceptibility and phenotypes in humans remains a considerable challenge. Currently, the lack of a definition between what is healthy and what is a dysbiotic gut microbiome limits research. Nevertheless, although clear proof-of-concept of causality is still lacking, there is an increasingly evident need to understand the microbial basis of IBD at the microbial strain, genomic, epigenomic, and functional levels and in specific clinical contexts. Recent information on the role of diet and novel environmental risk factors affecting the gut microbiome has direct implications for the immune response that impacts the development of IBD. The complexity of IBD pathogenesis, involving multiple distinct elements, suggests the need for an integrative approach, likely utilizing computational modeling of molecular datasets to identify more specific therapeutic targets.

Indexed as

Colitis, UlcerativeCrohn DiseaseGastrointestinal MicrobiomeInflammatory Bowel DiseasesDysbiosisHumansepigeneticsgut dysbiosisimmunomodulationinflammationinflammatory bowel disease

Identifiers

PMID35408838
PMCPMC8998182
OpenAlexW4223576130

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.