ReviewMolecular biology reports2026
Inflammasomes in digestive diseases: mechanisms and therapeutic potential.
Review in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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
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0 citing papers in PubMed.
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Authors and funding
10 authors.
Funding
Abstract
Inflammasomes are key multiprotein complexes in the innate immune system, playing crucial role in maintaining immune homeostasis and responding to pathogen invasion. Recent researches have increasingly unveiled the intricate and pivotal role of inflammasomes in the onset and progression of digestive diseases. This article provides a comprehensive review of the biological basis of inflammasomes, conducts an in-depth analysis of their relationship with the pathophysiological characteristics of digestive diseases, and elucidates the dual-edged nature of inflammasomes in modulating disease progression, tissue damage, and repair. We specifically highlight their activation processes, signaling pathways, and roles in the pathogenesis and pathological processes of common digestive disorders such as inflammatory bowel disease (IBD), gastritis, liver disease, and pancreatitis. Additionally, the article provides a detailed discussion of therapeutic strategies targeting inflammasomes and their potential clinical applications. In summary, targeting inflammasomes provides a new perspective and potential therapeutic approach for the treatment of digestive diseases.
Indexed as
Identifiers
42390729What 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.