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FGL2-induced metabolic dysregulation in enteric neural crest cells provides insight into Hirschsprung disease pathogenesis

Year: 2025

Type: article

Abstract: experiments using primary ENCCs isolated from embryonic mouse colon showed that FGL2 stimulation increased ENCC apoptosis. Mechanistically, FGL2 enhances oxidative phosphorylation (OXPHOS) via the activation of the JAK2-STAT3 signaling pathway, leading to reactive oxygen species (ROS) accumulation and subsequent apoptosis. Overall, these findings identify FGL2 as a potential pathogenic factor in HSCR that impacts ENCC survival and provide mechanistic insight into the metabolic regulation of ENCCs in the context of HSCR.

Source: iScience

DOI: 10.1016/j.isci.2025.113423

Authors: Jichang Han, Xiaoyang Liu, Yixuan Wang, Qiongqian Xu, Dong Sun, Xintao Zhang, Xixi He, Chuncan Ma, Xue Ren, Jian Wang, Yaru Mou, Qiangye Zhang, Dongming Wang, Weijing Mu, Peimin Hou, Aiwu Li

Institutions: Shandong University, Qilu Hospital of Shandong University, Shandong Provincial Hospital, Shandong First Medical University

Language: English

Topic: Congenital gastrointestinal and neural anomalies

Subfield: Surgery

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: gold

Estimated APC paid: $3,240

Funders: Shandong University, Taishan Scholar Foundation of Shandong Province, National Natural Science Foundation of China, Natural Science Foundation of Hunan Province, Natural Science Foundation of Shandong Province, Taishan Scholar Foundation of Shandong Province

Awards: G2301923881, G2574248110, G2960324067, G309909891, G3179668467, G36325110, G4140433530, G8650934365

OpenAlex ID: W4413478382

FWCI:

Cites: 30

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Related to: 10