©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Diabetes. Apr 15, 2025; 16(4): 101994
Published online Apr 15, 2025. doi: 10.4239/wjd.v16.i4.101994
Published online Apr 15, 2025. doi: 10.4239/wjd.v16.i4.101994
Exploring a novel mechanism for targeting β-arrestin-2 in the management of diabetic nephropathy
Na Liu, Wei-Tao Yan, Kun Xiong, Department of Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha 410013, Hunan Province, China
Author contributions: Liu N wrote the original draft; Yan WT reviewed and edited the manuscript; Xiong K was the senior author and provided supervision and validation of the writing; All authors have read and agreed to the published version of the manuscript.
Supported by National Natural Science Foundation of China, No. 82303047, No. 82372507, No. 82172196 and No. 32401046; and Natural Science Foundation of Hunan Province, No. 2022JJ40801.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Kun Xiong, PhD, Professor, Department of Anatomy and Neurobiology, School of Basic Medical Science, Central South University, No. 172 Tongzipo Road, Changsha 410013, Hunan Province, China. xiongkun2001@163.com
Received: October 14, 2024
Revised: January 4, 2025
Accepted: February 10, 2025
Published online: April 15, 2025
Processing time: 139 Days and 21.3 Hours
Revised: January 4, 2025
Accepted: February 10, 2025
Published online: April 15, 2025
Processing time: 139 Days and 21.3 Hours
Core Tip
Core Tip: Diabetic nephropathy (DN), a complication of diabetes mellitus, poses significant challenges in the management. Liu et al observed that β-arrestin-2 deteriorates DN through inducing endoplasmic reticulum (ER) stress, and inhibiting β-arrestin-2 may protect glomerular endothelial cells and mitigate DN progression by curbing ER stress. This research underscores the significance of ER stress in DN and reveals an innovative molecular pathway involving β-arrestin-2 that may contribute to DN progression, offering potential targets for therapeutic interventions. Nevertheless, further clinical validation and investigation are necessary to confirm the clinical application of these findings.