ReviewCells2020
Interplay between Cellular and Molecular Mechanisms Underlying Inflammatory Bowel Diseases Development-A Focus on Ulcerative Colitis.
Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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.
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.
Who cites it
25 citing papers in PubMed, 47 citations in OpenAlex.
- Photodynamic therapy-induced inflammation and adverse effects: An updated review.Biomedical journal · 2026Review
- ceRNA Network Dynamics in Inflammatory Bowel Disease: The LncRNA-miRNA-mRNA Axis in Intestinal Homeostasis and Inflammation.Cell biochemistry and biophysics · 2026Review
- Endoplasmic reticulum stress as a mechanistic link between nutrition and inflammatory bowel disease.Frontiers in nutrition · 2026Review
- Endoplasmic reticulum stress in gut inflammation: Implications for ulcerative colitis and Crohn's disease.World journal of gastroenterology · 2025Review
- Article
- Dihydromyricetin Improves Ulcerative Colitis by Suppressing NLRP3 Inflammasome Activation Caused by Dysbiosis of Gut Microbiota.Journal of inflammation research · 2025Article
- The Multiple Roles of Heat Shock Proteins in the Development of Inflammatory Bowel Disease.Current molecular medicine · 2025Review
- Exploration and verification a 13-gene diagnostic framework for ulcerative colitis across multiple platforms via machine learning algorithms.Scientific reports · 2024Article
- Article
- Potential diagnostic markers and therapeutic targets for non-alcoholic fatty liver disease and ulcerative colitis based on bioinformatics analysis and machine learning.Frontiers in medicine · 2024Article
- Network pharmacology andAnnals of medicine · 2022Article
- Perindopril/Ambrosin Combination Mitigates Dextran Sulfate Sodium-Induced Colitis in Mice: Crosstalk between Toll-Like Receptor 4, the Pro-Inflammatory Pathways, and SIRT1/PPAR-γ Signaling.Pharmaceuticals (Basel, Switzerland) · 2022Article
- SUCNR1 Mediates the Priming Step of the Inflammasome in Intestinal Epithelial Cells: Relevance in Ulcerative Colitis.Biomedicines · 2022Article
- Integrative computational approach identifies immune-relevant biomarkers in ulcerative colitis.FEBS open bio · 2022Article
- Identification of Potential Biomarkers and Immune Infiltration Characteristics in Ulcerative Colitis by Combining Results from Two Machine Learning Algorithms.Computational and mathematical methods in medicine · 2022Article
- Advances of Heat Shock Family in Ulcerative Colitis.Frontiers in pharmacology · 2022Review
- Endoplasmic Reticulum Stress of Gut Enterocyte and Intestinal Diseases.Frontiers in molecular biosciences · 2022Review
- NLRP3 inflammasome in digestive diseases: From mechanism to therapy.Frontiers in immunology · 2022Review
- Mechanism of M2 macrophage-derived extracellular vesicles carrying lncRNA MEG3 in inflammatory responses in ulcerative colitis.Bioengineered · 2021Article
- Characteristics of immune cell infiltration and associated diagnostic biomarkers in ulcerative colitis: results from bioinformatics analysis.Bioengineered · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory bowel diseases (IBD) are defined by the continuous inflammation of the gastrointestinal tract. During inflammation, the number of pathogens in the intestinal epithelium increases, leading to inflammasome assembly. Inflammasome activation is meant to protect the intestinal epithelial barrier from further damage by maintaining homeostasis. Although its purpose is to protect the cells, excessive nucleotide-binding oligomerization domain-like receptor and pyrin domain-containing protein 3 (NLRP3) inflammasome assembly is responsible for the synthesis of a high number of pro-inflammatory cytokines. The activation of two crucial pathways, autophagy process, and unfolded protein response, is initiated for restoring homeostasis. Aberrant expression of miRNAs and lncRNAs also interfere with the pathogenic mechanisms of IBD, as these non-coding transcripts play key roles in regulation of biological processes, such as inflammation and immunity. This review thoroughly describes the cellular and molecular mechanism that trigger and perpetuate inflammation in ulcerative colitis (UC) patients.
Indexed as
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What OpenQuestion holds
Registered trials
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.