ReviewBiomolecules & therapeutics2025
Chitinase-3-Like Protein 1 as a Therapeutic Target for Inflammatory Diseases.
Review in Biomolecules & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
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
3 citing papers in PubMed.
- Redefining CHI3L1: Therapeutic Opportunities at the Crossroads of Immune Suppression and Disease Progression.Medicinal research reviews · 2026Review
- Structure-Guided Optimization of CHI3L1 Modulators Reveals G721-0377 as a Lead Compound for Restoring Astrocyte Function in Alzheimer's Disease.ACS bio & med chem Au · 2026Article
- Translational insights into interleukin-driven macrophage polarization as diagnostic biomarkers for atopic dermatitis-a narrative review.Frontiers in molecular biosciences · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chitinase-3-like protein 1 (CHI3L1) is a secreted glycoprotein involved in macrophage polarization, apoptosis, and inflammation, and carcinogenesis. The expression of CHI3L1 is significantly increased in various inflammatory and immunological diseases, such as rheumatoid arthritis, Alzheimer's disease, and atopic dermatitis. Several studies suggest that CHI3L1 may be a viable therapeutic target for these diseases, given its ability to release various pro-inflammatory cytokines, including interleukin (IL)-1β, IL-4, IL-6, IL-13, tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ). Therefore, CHI3L1 likely plays a role in the development of a broad spectrum of inflammatory diseases. However, the precise pathophysiological and pharmacological mechanisms by which CHI3L1 contributes to these diseases remain to be fully elucidated. This review synthesizes recent findings on the functional roles of CHI3L1 across diverse inflammatory conditions, highlighting its involvement in critical signaling pathways. Moreover, preclinical research underscores the therapeutic potential of CHI3L1 inhibition. Thus, targeted CHI3L1 interventions represent a compelling therapeutic strategy warranting further clinical exploration and validation.
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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.