IER3 drives the transition from sepsis-associated AKI to CKD by suppressing the mitochondrial translocation of PRDX5.
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ABSTRACT: Sepsis-associated acute kidney injury (SAKI) is a severe condition associated with high mortality and long-term complications. Currently, there is no effective strategy to halt AKI chronicization. Stress-induced senescence of renal tubular epithelial cells (RTECs) is a pivotal driving mechanism in the AKI-CKD transition. Previous scRNA-seq revealed that the expression of immediate early response gene 3 (IER3) was markedly upregulated in the senescent RTECs of patients with AKI and that the IER3+RTEC subpopulation exhibited diminished differentiation potential and impaired self-renewal capacity. However, the role of IER3 in RTEC stress-induced senescence following AKI remains unclear. In this study, we found that knockout of IER3 reduced mortality rates, alleviated renal injury,
SUBMITTER: Dou Q
PROVIDER: S-EPMC12686328 | biostudies-literature | 2025 Dec
REPOSITORIES: biostudies-literature
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