Publication Name	World Journal of Gastroenterology
Manuscript ID	108814
Country	China

Category	Gastroenterology & Hepatology
Manuscript Type	Letter to the Editor
Article Title	Metabolic dysfunction-associated steatotic liver disease: Mechanisms, metabolic reprogramming, and therapeutic insights
Manuscript Source	Unsolicited Manuscript
All Author List	Wan-Qi Yang, Ling-Ling Xue and Jing-Lin Wang
Funding Agency and Grant Number
Corresponding Author	Jing-Lin Wang, PhD, Researcher, Division of Hepatobiliary and Transplantation Surgery, Department of General Surgery, Nanjing Drum Tower Hospital, Clinical College of Nanjing University of Chinese Medicine, No. 321 Zhongshan Road, Nanjing 210008, Jiangsu Province, China. cw20120817@163.com
Key Words	Metabolic dysfunction-associated steatotic liver disease; Aging; Vitamin D receptor; Metabolic reprogramming; Ferroptosis
Core Tip	Metabolic dysfunction-associated steatotic liver disease (MASLD) is a progressive disorder intricately linked to aging through shared pathological pathways. The core mechanism driving aging-aggravated MASLD involves vitamin D receptor (VDR) dysregulation, which amplifies hepatic lipotoxicity by disrupting lipid metabolism and inducing ferroptosis. Although metabolic reprogramming initially serves as an adaptive response to stress, its dysregulation in aging accelerates inflammation and fibrosis. However, precisely targeting the VDR–p53 axis to modulate mitochondrial function and ferroptotic susceptibility, while balancing metabolic adaptation and cell death, remains a critical therapeutic challenge for halting disease progression.
Citation	Yang WQ, Xue LL, Wang JL. Metabolic dysfunction-associated steatotic liver disease: Mechanisms, metabolic reprogramming, and therapeutic insights. World J Gastroenterol 2025; In press

Received	2025-04-24 11:47
Peer-Review Started	2025-04-24 11:48
To Make the First Decision
Return for Revision	2025-05-30 18:29
Revised	2025-06-06 08:10
Second Decision	2025-06-26 02:36
Accepted by Journal Editor-in-Chief
Accepted by Executive Editor-in-Chief	2025-06-26 06:42
Articles in Press	2025-06-26 06:42
Publication Fee Transferred
Edit the Manuscript by Language Editor
Typeset the Manuscript

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