ReviewInternational journal of molecular sciences2025
Galectin-3-Insights from Inflammatory Bowel Disease and Primary Sclerosing Cholangitis.
Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026Review
- Article
- Galectin-3-A Multifunctional Molecule and a Key Player in Health and Disease.Molecules (Basel, Switzerland) · 2026Review
- Review
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory bowel disease (IBD) and primary sclerosing cholangitis (PSC) are related diseases with poorly understood pathophysiology. While therapy options for IBD have increased, treatment options for PSC remain limited. Galectin-3 is a multifunctional lectin expressed in intestinal epithelial cells, and is abundant in immune cells such as macrophages, with roles in cell adhesion, apoptosis, inflammation and fibrosis being associated with IBD and PSC disease development and progression. In addition, galectin-3 is also a visceral fat-derived protein whose systemic levels are increased in obese individuals, the latter correlating with a poorer prognosis in IBD and PSC patients. On the other hand, decreased galectin-3 expression in the inflamed mucosal tissues of mice and patients with IBD possibly indicate a protective role of this lectin in IBD. However, galectin-3 loss or inhibition is protective in most animal models of liver fibrosis but exacerbates the severity of autoimmune liver disease. Hence, with PSC being a slowly progressing autoimmune hepatobiliary disease closely related to IBD, further studies evaluating galectin-3 as a therapeutic target or biomarker for the severity of IBD and the occurrence of PSC are still needed. This review summarizes studies that have analyzed expression patterns and functions of galectin-3 in IBD and PSC. Current evidence suggests that strategies to block galectin-3 are not advised for patients with IBD and PSC-IBD.
Indexed as
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.