ReviewBiomedicines2025
Inflammatory Bowel Disease: Understanding Therapeutic Effects of Distinct Molecular Inhibitors as the Key to Current and Future Advanced Therapeutic Strategies.
Review in Biomedicines, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Crohn's Disease and Ulcerative Colitis: From Pathophysiology to Novel Therapeutic Approaches (3rd Edition).Biomedicines · 2026Article
- Interleukin-23 Inhibitors in Inflammatory Bowel Disease.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026Review
- Current Perspectives on the Inflammatory Bowel Disease Pathogenesis of Microbiota and the Gut-Brain Axis, and Emerging Therapeutics.Biomedicines · 2026Review
- IRG1-itaconate axis in immunometabolism: mechanistic roles and therapeutic potential in inflammatory diseases.Frontiers in immunology · 2026Review
- Case Report: Interleukin-23 blockade achieves sustained remission in Niemann-Pick type C-associated Crohn's disease refractory to anti-tumor necrosis factor therapy.Frontiers in immunology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of Inflammatory Bowel Disease is complex and not completely understood, resulting from multifactorial interactions between genetic predisposition, environmental triggers, and dysregulation of both innate and adaptive immune responses. Cytokines, produced by dysregulated immune cells, trigger chronic intestinal inflammation leading to tissue damage, carcinogenesis, and disease perpetuation. Current advanced therapies-including tumor necrosis factor (TNF)-α antagonists, adhesion and trafficking inhibitors (such as anti-integrin agents and sphingosine-1-phosphate receptor modulators), interleukin inhibitors, and Janus kinase inhibitors-have improved patient outcomes, but targeting a single inflammatory pathway is often insufficient for long-term disease control. To further improve therapeutic efficacy, novel approaches are under investigation, including advanced combination therapies that simultaneously inhibit multiple pro-inflammatory pathways and microbiome-based treatments to restore intestinal homeostasis. In this evolving therapeutic scenario, precision medicine and advanced combination therapies appear promising for breaking through the current therapeutic ceiling. This review highlights current knowledge on the role of cytokines in IBD pathogenesis and explores how their modulation can modify and control disease course.
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Identifiers
What Socratic 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 Socratic graph.