Publication Name	World Journal of Gastroenterology
Manuscript ID	113647
Country	China

Category	Gastroenterology & Hepatology
Manuscript Type	Basic Study
Article Title	Allyl isothiocyanate ameliorates metabolic dysfunction-associated steatotic liver disease via vitamin D receptors in hepatocytes
Manuscript Source	Unsolicited Manuscript
All Author List	Ting Gao, Kang-Peng Zhong, Jun-Zhuo Wang, Yi Chen and Chun-Xiao Li
Funding Agency and Grant Number	Funding Agency Grant Number Natural Science Foundation of Zhejiang Province No. LQ22H030001 Natural Science Foundation of Ningbo No. 2024J474 Ningbo Top Medical and Health Research Program No. 2023020612 Project of Ningbo Leading Medical and Healthy Discipline No. 2022-S04
Corresponding Author	Chun-Xiao Li, PhD, Department of Gastroenterology, The First Affiliated Hospital of Ningbo University, No. 59 Liuting Street, Haishu District, Ningbo 315010, Zhejiang Province, China. 11418130@zju.edu.cn
Key Words	Allyl isothiocyanate; Metabolic dysfunction-associated steatotic liver disease; Vitamin D receptor; Fatty acid β-oxidation; Lipid synthesis
Core Tip	Metabolic dysfunction-associated steatotic liver disease (MASLD) denotes a continuum of disorders unified by hepatic steatosis and can affect approximately one quarter of the global population, reaching up to 75% among individuals with obesity. This work seeks to define the functional contribution and mechanism of allyl isothiocyanate (AITC) in mitigating MASLD via the vitamin D receptor (VDR). In an in vitro MASLD model, AITC activates VDR through hepatocyte nuclear factor 4 alpha/microsomal triglyceride transfer protein/apolipoprotein B signaling, thereby reducing lipid accumulation and insulin resistance while promoting fatty acid β-oxidation. Taken together, these results show the therapeutic promise of AITC in MASLD.
Citation	Gao T, Zhong KP, Wang JZ, Chen Y, Li CX. Allyl isothiocyanate ameliorates metabolic dysfunction-associated steatotic liver disease via vitamin D receptors in hepatocytes. World J Gastroenterol 2025; In press

Received	2025-09-01 08:55
Peer-Review Started	2025-09-01 08:57
To Make the First Decision
Return for Revision	2025-10-11 06:53
Revised	2025-10-24 06:21
Second Decision	2025-11-19 02:35
Accepted by Journal Editor-in-Chief
Accepted by Executive Editor-in-Chief	2025-11-19 09:27
Articles in Press	2025-11-19 09:27
Publication Fee Transferred	2025-10-27 13:07
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Typeset the Manuscript

ISSN	1007-9327 (print) and 2219-2840 (online)
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