Publication Name	World Journal of Diabetes
Manuscript ID	114679
Country	China

Category	Urology & Nephrology
Manuscript Type	Basic Study
Article Title	Hyperoside attenuates diabetic nephropathy by activating the Nrf2/SLC7A11/GPX4 axis to restrain ferroptosis
Manuscript Source	Unsolicited Manuscript
All Author List	Chao Liu, Yan Li, Yuan Zhang, Ming Gao and Shi-Feng Yang
Funding Agency and Grant Number
Corresponding Author	Shi-Feng Yang, MD, Department of Nephrology, The First Affiliated Hospital of Xi’an Jiaotong University, No. 277 Yanta West Road, Xi’an 710061, Shaanxi Province, China. jeffysy@126.com
Key Words	Hyperoside; Diabetic nephropathy; Ferroptosis; Nrf2; SLC7A11; GPX4; Oxidative stress
Core Tip	This study, for the first time, demonstrates that hyperoside, a natural flavonoid, protects against diabetic nephropathy by suppressing ferroptosis via activation of the Nrf2/SLC7A11/GPX4 antioxidant axis. In high-glucose-challenged HK-2 cells, hyperoside restored glutathione, reduced lipid reactive oxygen species and Fe2+ accumulation, and improved cell viability, effects comparable to ferrostatin-1. In streptozotocin-induced diabetic nephropathy rats, hyperoside ameliorated renal dysfunction and histologic injury while upregulating Nrf2/SLC7A11/GPX4. These findings provide mechanistic and experimental support for hyperoside as a potential therapeutic candidate for diabetic nephropathy.
Citation	Liu C, Li Y, Zhang Y, Gao M, Yang SF. Hyperoside attenuates diabetic nephropathy by activating the Nrf2/SLC7A11/GPX4 axis to restrain ferroptosis. World J Diabetes 2026; In press

Received	2025-09-26 04:23
Peer-Review Started	2025-09-29 08:09
First Decision by Editorial Office Director	2025-10-21 06:29
Return for Revision	2025-10-21 06:29
Revised	2025-11-01 12:42
Publication Fee Transferred	2025-11-03 08:59
Second Decision by Editor	2025-12-03 09:42
Second Decision by Editor-in-Chief
Final Decision by Editorial Office Director	2026-02-05 07:02
Articles in Press	2026-02-05 07:02
Edit the Manuscript by Language Editor
Typeset the Manuscript

ISSN	1948-9358 (online)
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