ReviewMolecular medicine reports2025
Progress in targeting the NLRP3 signaling pathway for inflammatory bowel disease (Review).
Review in Molecular medicine reports, 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.
- Elevated caspase 3 expression correlates with severe inflammation in Crohn's disease.European journal of histochemistry : EJH · 2026Article
- Bioengineering Interventions to Enhance the Capacity of the Gut Microbiota in Controlling Food Allergies.Life (Basel, Switzerland) · 2026Review
- Macrophage-driven inflammation in inflammatory bowel disease: mechanisms and therapeutic opportunities.Frontiers in bioengineering and biotechnology · 2026Review
- Inflammatory bowel disease and renal disorders: from clinical associations to shared mechanisms and management strategies.Frontiers in immunology · 2026Review
- Molecular Evolution of the NLR Gene Family Reveals Diverse Innate Immune Strategies in Bats.Biomolecules · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory caspases pro‑inflammatory cytokines, such as IL‑1β IL‑18, constitute a critical part in the modulation of innate immune responses by the nucleotide‑binding domain leucine‑rich repeat protein (NLRP)3 inflammasome. The NLRP3 inflammasome, a cytosolic complex, is composed of three distinct classes of proteins‑sensor complexes, adaptor proteins, cysteine proteases. It is well‑established that this pathway can powerfully influence the pathophysiology of autoimmune diseases along with an association of a plethora of inflammatory conditions. Therefore, it is of great significance to elucidate the mechanisms through which NLRP3 participates in disease development functions as a potential target for pharmacological intervention. The present review discussed the function role of the NLRP3 inflammasome in inflammatory bowel disease and described the structure assembly and activation mechanism of the NLRP3 inflammasome. Additionally, it explored novel clinical viewpoints and therapeutic advances in targeted NLRP3 inflammasome therapy. In conclusion, the present review offered a comprehensive overview of inflammatory bowel disease and the NLRP3 inflammasome. It is expected to serve as a guide for future research, potentially leading to improved patient outcomes. The present review has been submitted as a pre‑print (https://papers.ssrn.com/sol3/papers.cfm?abstract_id=4962722).
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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.