ReviewAnnals of gastroenterology
Signaling pathways associated with bone loss in inflammatory bowel disease.
Review in Annals of gastroenterology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 6 citations in OpenAlex.
- Bone targeted microenvironment actuated engineered exosomes for precision therapy of IBD associated bone loss.Bioactive materials · 2026Article
- Dried Ginger Milk Extract Alleviates Inflammatory Bowel Disease-Associated Bone Loss via Gut Microbiota-Metabolite Remodeling and MEK/ERK Inhibition.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Cell-Free DNA-Based Theranostics for Inflammatory Disorders.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Bone turnover markers in patients with inflammatory bowel disease in remission: a cross-sectional comparison of anti-TNFα therapy with conventional maintenance therapy.Frontiers in medicine · 2026Article
- The brain-bone-gut axis: a microbial bridge underlying multisystem comorbidities.Frontiers in endocrinology · 2026Review
- Article
- The Role of the Myokine Irisin in the Protection and Carcinogenesis of the Gastrointestinal Tract.Antioxidants (Basel, Switzerland) · 2024Review
- Impact of Folate Intake on Bone Mineral Density in Patients with Inflammatory Bowel Disease.Nutrients · 2023Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract characterized in many patients by extraintestinal manifestations. One of the most common comorbidities seen in IBD patients is a significant reduction in their bone mass. The pathogenesis of IBD is mainly attributed to the disrupted immune responses in the gastrointestinal mucosa and putative disruptions in the gut microbiomes. The excessive inflammation of the gastrointestinal tract activates different systems, such as the RANKL/RANK/OPG and the Wnt pathways linked with bone alterations in IBD patients, thereby suggesting a multifactorial etiology. The mechanism responsible for the reduced bone mineral density in IBD patients is thought to be multifactorial, and, so far, the principal pathophysiological pathway has not been well established. However, in recent years, many investigations have increased our understanding of the effect of gut inflammation on the systemic immune response and bone metabolism. Here, we review the main signaling pathways associated with altered bone metabolism in IBD.
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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.