2. Academic Validation
  3. Exploring the Protective Role and Regulation of Prdx6 in Cisplatin-Induced AKI

Exploring the Protective Role and Regulation of Prdx6 in Cisplatin-Induced AKI

  • Clin Exp Pharmacol Physiol. 2026 Jan;53(1):e70093. doi: 10.1111/1440-1681.70093.
Xianzhe Li 1,  Jinbo Yu 1 2 3 4,  Shi Cheng 1,  Yaqiong Wang 1 2 3 4 5,  Xiaoqiang Ding 1 2 3 4 5
Affiliations

Affiliations

  • 1 Department of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China.
  • 2 Shanghai Medical Center of Kidney Disease, Shanghai, China.
  • 3 Shanghai Key Laboratory of Kidney and Blood Purification, Shanghai, China.
  • 4 Hemodialysis Quality Control Center of Shanghai, Shanghai, China.
  • 5 Kidney and Dialysis Institute of Shanghai, Shanghai, China.
PMID: 41267204 DOI: 10.1111/1440-1681.70093
Abstract

Cisplatin (CDDP) is a widely used chemotherapeutic agent that induces nephrotoxicity by generating excessive Reactive Oxygen Species (ROS), leading to oxidative stress, inflammation and Apoptosis in renal proximal tubular cells. Peroxiredoxin 6 (Prdx6), an antioxidant enzyme, plays a crucial role in maintaining ROS homeostasis by degrading hydroperoxides; however, its role in CDDP-induced acute kidney injury (CIAKI) remains unclear. In this study, a CIAKI model was established using CDDP treatment in vivo (C57BL/6 mice) and in vitro (PTECs) with or without Prdx6 overexpression (Prdx6 OE). CDDP treatment significantly increased ROS levels, while Prdx6 OE attenuated oxidative stress, Apoptosis and renal tubular damage. Furthermore, we found that Prdx6 expression was regulated by Nuclear factor erythroid 2-related factor 2 (Nrf2), suggesting a mechanistic link between Nrf2 and Prdx6 in CIAKI. These findings indicate that Prdx6 plays a protective role in CDDP-induced nephrotoxicity by modulating oxidative stress and Apoptosis, and highlight its potential as a therapeutic target.

Keywords

CDDP; CIAKI; Nrf2; Prdx6.

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