Observational analysis found low DUSP2 levels correlate with high HIF-1α in AKI patients, suggesting DUSP2 may protect renal cells.
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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Chu et al. (2025) studied this question.
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