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Expression characteristics of dual-specificity phosphatase 2 and hypoxia-inducible factor-1α in acute kidney injury and preliminary study of the effect of dual-specificity phosphatase 2 on HK-2 cells.

作者信息

Chu Xueqian, Xue Songmin, Lin Lanyan, Huang Xuan, Chen Sisi, Adeli Wulaer, Tuohetiyaer Zulibiya, Li Suhua, Lu Chen

机构信息

Nephrology Disease Center, The First Affiliated Hospital of Xinjiang Medical University, State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Urumqi, Xinjiang, China.

Xinjiang Clinical Research Center of Renal Replacement Therapy, Urumqi, Xinjiang, China.

出版信息

Exp Physiol. 2025 Sep 2. doi: 10.1113/EP092493.

Abstract

Acute kidney injury (AKI) is a global health problem with significant long-term harm if the prognosis is poor. Dual-specificity phosphatase 2 (DUSP2) is involved in key regulatory pathways in several disease processes, but its function in renal pathophysiology is unclear. The expression levels of DUSP2 in the peripheral blood of AKI and non-AKI patients were first examined. The expression characteristics of DUSP2 and hypoxia-inducible factor-1α (HIF-1α) in AKI conditions were analysed in renal tissues from AKI patients and different AKI model mice. Human renal tubular epithelial cells (HK-2) were utilized for in vitro experiments to investigate the effects of overexpression of DUSP2 on cell proliferation, apoptosis and HIF-1α levels under hypoxia-reoxygenation conditions. DUSP2 showed low expression in the peripheral blood serum of AKI patients. In the renal tissues of patients and mouse models of AKI, DUSP2 expression was significantly lower, and HIF-1α expression was significantly higher. Under hypoxia-reoxygenation conditions, DUSP2 overexpression promoted HK-2 cell proliferation, inhibited apoptosis and suppressed HIF-1α expression. The present study demonstrated a significant correlation between DUSP2 and HIF-1α expression in the context of AKI and revealed the protective effect of DUSP2 overexpression on renal tubular epithelial cells under hypoxia-reoxygenation, which provides a new better understanding of AKI.

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