Publication Name	World Journal of Diabetes
Manuscript ID	112027
Country	China

Category	Cardiac & Cardiovascular Systems
Manuscript Type	Basic Study
Article Title	Microtubule affinity-regulating kinase 4 exacerbates diabetic cardiomyopathy by inhibiting UNC-51-like kinase 1-mediated mitochondrial autophagy
Manuscript Source	Unsolicited Manuscript
All Author List	Yi Wu, Wei-Yi Wang, Jing-Qi Zhang, Sai Wang, Zhi Zeng, Lu Fu and Bin Li
Funding Agency and Grant Number	Funding Agency Grant Number Health and Wellness Science and Technology Project of Hubei Province WJ2025Q012
Corresponding Author	Bin Li, Academic Fellow, Associate Chief Physician, The Clinical Research Center for Acute Myocardial Infarction of Hubei Province, Xianning Central Hospital, No. 228 Jingui Road, Xianning 437000, Hubei Province, China. lbxnszxyy0405@163.com
Key Words	Microtubule affinity-regulating kinase 4; Diabetic cardiomyopathy; Mitochondrial autophagy; UNC-51-like kinase 1; Microtubule-associated protein 1 light chain 3B
Core Tip	This study explored the role of microtubule affinity-regulating kinase 4 (MARK4) in diabetic cardiomyopathy (DCM). The results showed that the MARK4 level was significantly elevated in DCM mice. Down-regulation of MARK4 could alleviate myocardial injury and enhance mitochondrial autophagy function. By up-regulating UNC-51-like kinase 1, the down-regulation of MARK4 promotes mitochondrial autophagy and protects cardiac function. This study reveals the significance of MARK4 as a potential therapeutic target for DCM, providing new ideas for protecting the myocardium of diabetic patients.
Citation	Wu Y, Wang WY, Zhang JQ, Wang S, Zeng Z, Fu L, Li B. Microtubule affinity-regulating kinase 4 exacerbates diabetic cardiomyopathy by inhibiting UNC-51-like kinase 1-mediated mitochondrial autophagy. World J Diabetes 2025; In press

Received	2025-07-17 04:12
Peer-Review Started	2025-07-21 00:23
To Make the First Decision
Return for Revision	2025-08-08 08:00
Revised	2025-09-04 03:07
Second Decision	2025-11-28 03:01
Accepted by Journal Editor-in-Chief
Accepted by Executive Editor-in-Chief	2025-11-28 07:12
Articles in Press	2025-11-28 07:12
Publication Fee Transferred	2025-09-08 07:32
Edit the Manuscript by Language Editor
Typeset the Manuscript

ISSN	1948-9358 (online)
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