Li B. Microglial voltage-gated proton channel 1 ablation in diabetic mice mitigates diabetes-driven demyelination and cognitive decline. World J Psychiatry 2025; 15(9): 109363 [PMID: 40933142 DOI: 10.5498/wjp.v15.i9.109363]
Corresponding Author of This Article
Bin Li, PhD, Full Professor, Department of Comparative Medicine, Yangzhou University, No. 88 Daxue South Road, Yangzhou 225009, Jiangsu Province, China. lib111701@163.com
Research Domain of This Article
Cell Biology
Article-Type of This Article
Letter to the Editor
Open-Access Policy of This Article
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World J Psychiatry. Sep 19, 2025; 15(9): 109363 Published online Sep 19, 2025. doi: 10.5498/wjp.v15.i9.109363
Microglial voltage-gated proton channel 1 ablation in diabetic mice mitigates diabetes-driven demyelination and cognitive decline
Bin Li
Bin Li, Department of Comparative Medicine, Yangzhou University, Yangzhou 225009, Jiangsu Province, China
Bin Li, Center for Integrative Physiology and Molecular Medicine, University of Saarland, Homburg 66424, Saarland, Germany
Author contributions: Li B contributed to the manuscript writing, reviewing, editing, and participated in the formal analysis, conceptualization, project administration.
Supported by the Top-Level Talents Support Program of Yangzhou University; “Lv Yang Jin Feng” Outstanding Doctor of Yangzhou, No. YZLYJFJH2023YXBS169; and Natural Science Foundation of Jiangsu Province, No. BK20240907.
Conflict-of-interest statement: The author reports no relevant conflicts of interest for this article.
Corresponding author: Bin Li, PhD, Full Professor, Department of Comparative Medicine, Yangzhou University, No. 88 Daxue South Road, Yangzhou 225009, Jiangsu Province, China. lib111701@163.com
Received: May 13, 2025 Revised: May 23, 2025 Accepted: July 14, 2025 Published online: September 19, 2025 Processing time: 105 Days and 20.7 Hours
Core Tip
Core Tip: Building upon the groundbreaking work by Li et al who demonstrated that microglial voltage-gated proton channel 1 knockout effectively mitigates neuroinflammation, preserves myelin integrity, and rescues memory deficits in diabetic mouse models, our suggestions focus on advancing this research trajectory. We propose implementing longitudinal assessments to track chronic impacts, utilizing cell-type-specific approaches for mechanistic clarity, and pursuing pharmacological translation for therapeutic potential. To systematically guide these efforts, we provide structured tabulated overviews detailing the study’s strengths, acknowledging its inherent limitations, and outlining specific strategic research pathways for future investigation.
