ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024
Gut Dysbiosis Drives Inflammatory Bowel Disease Through the CCL4L2-VSIR Axis in Glycogen Storage Disease.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Intestinal epithelial PIEZO1 regulates macrophage-to-myofibroblast transition via epithelial-derived TGF-α signaling in Crohn's disease.Cell communication and signaling : CCS · 2026Article
- Living Hydrogels: Harnessing Microorganism-Material Synergy for Next-Generation Therapeutics.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Advances of exosome regulating‑FXR to repair inflammatory bowel disease (Review).International journal of molecular medicine · 2025Review
- [Application of active glucose monitoring in the perioperative period of gastrointestinal endoscopy in children with glycogen storage disease type Ⅰb].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2025Article
- [Efficacy and safety of empagliflozin in the treatment of glycogen storage disease-associated inflammatory bowel disease].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2025Article
- Gastrointestinal complications of hepatic glycogen storage disease: a national survey questionnaire study in China.Orphanet journal of rare diseases · 2025Article
- CCL4L2 is a potential biomarker for differentiating central and peripheral vertigo.Frontiers in integrative neuroscience · 2025Article
- Gut Dysbiosis Drives Inflammatory Bowel Disease Through the CCL4L2-VSIR Axis in Glycogen Storage Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
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49 authors.
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Abstract
Patients with glycogen storage disease type Ib (GSD-Ib) frequently have inflammatory bowel disease (IBD). however, the underlying etiology remains unclear. Herein, this study finds that digestive symptoms are commonly observed in patients with GSD-Ib, presenting as single or multiple scattered deep round ulcers, inflammatory pseudo-polyps, obstructions, and strictures, which differ substantially from those in typical IBD. Distinct microbiota profiling and single-cell clustering of colonic mucosae in patients with GSD are conducted. Heterogeneous oral pathogenic enteric outgrowth induced by GSD is a potent inducer of gut microbiota immaturity and colonic macrophage accumulation. Specifically, a unique population of macrophages with high CCL4L2 expression is identified in response to pathogenic bacteria in the intestine. Hyper-activation of the CCL4L2-VSIR axis leads to increased expression of AGR2 and ZG16 in epithelial cells, which mediates the unique progression of IBD in GSD-Ib. Collectively, the microbiota-driven pathomechanism of IBD is demonstrated in GSD-Ib and revealed the active role of the CCL4L2-VSIR axis in the interaction between the microbiota and colonic mucosal immunity. Thus, targeting gut dysbiosis and/or the CCL4L2-VISR axis may represent a potential therapy for GSD-associated IBD.
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