ALG10 Alleviates IBD-Related Intestinal Fibrosis by Modulating the TGF-β1/PI3K/Akt Signaling Pathway.

Authors

Mengmeng Yang, Xingshu Wei, Renhui Wu, Yuhui Wang, Xiaotian Xu

Published in

Digestive diseases and sciences. Jul 20, 2026. Epub Jul 20, 2026.

Abstract

To explore the role of asparagine-linked glycosylation 10 (ALG10) in intestinal fibrosis (IF) and elucidate its underlying molecular mechanisms.
Western 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^-/- mouse models were established, and primary colonic fibroblasts were isolated in vitro. Pathological changes and collagen deposition in colon tissues were evaluated via Masson's trichrome staining and H&E staining. RT-qPCR, Western blot, and ELISA were performed to measure the expression of IF-related markers. A TGF-β1-induced CCD-18Co cell model was established, and immunofluorescence was used to detect the fluorescence intensity of COL I and E-cadherin. The interaction mechanism between ALG10 and TGF-β1 was further explored by molecular docking, MD simulation, Co-IP and dual-luciferase reporter gene experiments.
Compared 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.
ALG10 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.

PMID:
42474621
Bibliographic data and abstract were imported from PubMed on 20 Jul 2026.

Read full publication at:
Please sign in to see all details.

Stats

1-terrible, 9-excellent. How would you rate this publication? Sign in in to submit your rating.

Post a comment

You need to be signed in to post comments. You can sign in here.

Comments

There are no comments yet.