ArticleDigestive diseases and sciences2026
ALG10 Alleviates IBD-Related Intestinal Fibrosis by Modulating the TGF-β1/PI3K/Akt Signaling Pathway.
Article in Digestive diseases and sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
purposeTo explore the role of asparagine-linked glycosylation 10 (ALG10) in intestinal fibrosis (IF) and elucidate its underlying molecular mechanisms.
methodsWestern blot and RT-qPCR were employed to detect ALG10 expression in a TNBS/DSS-induced mouse IF model and in primary colonic fibroblasts. TNBS/DSS-induced ALG10
resultsCompared with the WT group, ALG10 expression was significantly increased in the TNBS/DSS group. In both in vivo and in vitro models, ALG10 silencing markedly alleviated fibrosis severity and pathological damage, downregulated the expression of COL I and α-SMA, and upregulated E‑cadherin expression and significantly reduced the levels of p‑PI3K, p‑Akt, and the target genes FGF2 and p‑FoxO1/3a. Molecular docking, MD simulations, and Co-IP assays suggested that ALG10 potentially interacts with TGF-β1, while dual-luciferase reporter assays further demonstrated that ALG10 promotes TGF-β1 promoter activity.
conclusionALG10 acts as a key mediator promoting the progression of IF. Silencing ALG10 can alleviate IBD-related IF, a mechanism that may involve the regulation of the TGF‑β1/PI3K/Akt signaling pathway.
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