Evidence map›Paper›PMID 39185541›Full record

ReviewTissue barriers2025

Epithelial barrier dysfunction and microbial dysbiosis: exploring the pathogenesis and therapeutic strategies for Crohn's disease.

Tunç Akkoç

Abstract readReview
In one paragraph

Review in Tissue barriers, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

7 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
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

1 author.

Tunç AkkoçDepartment of Immunology, Marmara University School of Medicine, İstanbul, Türkiye.ORCID 0000-0001-9179-2805

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Crohn's disease (CD), a chronic gastrointestinal inflammatory disease, is becoming more widespread worldwide. Crohn's disease is caused by gut microbiota changes, genetics, environmental stresses, and immunological responses. Current treatments attempt to achieve long-term remission and avoid complications, delaying disease progression. Immunosuppressive measures and combination medicines should be started early for high-risk patients. These medicines monitor inflammatory indicators and adjust as needed. The epithelial barrier helps defend against physical, chemical, and immunological threats. When tissues' protective barrier breaks down, the microbiome may reach the layer underneath. Unbalanced microbial populations and inflammation impair healing and adjustment. Inflammatory cells infiltrating sensitive tissues aggravate the damage and inflammation. This approach promotes chronic inflammatory diseases. The epithelial barrier hypothesis states that hereditary and environmental variables cause epithelial tissue inflammation. This review focuses on how epithelial barrier break-down and microbial dysbiosis cause Crohn's disease and current advances in understanding the epithelial barrier, immune system, and microbiome. Additionally, investigate treatments that restore barrier integrity and promote microbial balance. Overall, it stresses the role of epithelial barrier failure and microbial dysbiosis in Crohn's disease development and discusses current advances in understanding the barrier, immunological responses, and microbiota.

Indexed as

Crohn DiseaseDysbiosisGastrointestinal MicrobiomeIntestinal MucosaAnimalsHumansCrohn’s disease pathogenesisepithelial barrier dysfunctionimmune responsesmicrobial dysbiosistherapeutic strategies

Identifiers

PMID39185541
PMCPMC12363530

What Socratic holds

Textmetadata
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 Socratic graph.