Abstract: SA-PO0258
Inhibiting CSDE1 Alleviates Renal Ischemia-Reperfusion Injury via Activating the PTEN/PI3K/Akt Pathway
Session Information
- AKI: Mechanisms - Cell Signaling
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 103 AKI: Mechanisms
Authors
- Tang, Rong, Xiangya Hospital Central South University, Changsha, Hunan, China
- Luo, Zengyuan, Xiangya Hospital Central South University, Changsha, Hunan, China
- Chen, Jinbiao, Xiangya Hospital Central South University, Changsha, Hunan, China
- Tang, Jieyu, Xiangya Hospital Central South University, Changsha, Hunan, China
- Wang, Zaiyu, Xiangya Hospital Central South University, Changsha, Hunan, China
Background
Acute kidney injury (AKI) has high incidence and poor prognosis with unclear mechanisms and lacks effective therapeutic targets. Most studies focus on transcriptional regulation in ischemia-reperfusion (I/R) kidney injury, whereas translational reprogramming remains poorly understood. As an RNA-binding protein, CSDE1 is critical for translational reprogramming. This study aimed to explore the role and mechanism of CSDE1 in AKI.
Methods
Single-cell RNA sequencing analyzed transcriptional profiles in kidneys from ischemic AKI patients. CSDE1 expression was validated by immunofluorescence and qRT-PCR, while serum and urinary CSDE1 levels in clinical cohorts were measured by ELISA. The I/R-AKI model and global CSDE1 knockout mice were employed. RNA sequencing was used to probe CSDE1 downstream mechanisms. The expression of PTEN, PI3K, p-PI3K, Akt, p-Akt, apoptosis and autophagy-related molecules was detected in I/R-AKI mice and hypoxia-reoxygenation cell model. TUNEL staining was applied to evaluate apoptosis.
Results
In ischemic AKI patient and I/R-AKI mice kidney, CSDE1 was upregulated in proximal tubular epithelial cells. Urinary CSDE1 was increased in AKI patients and positively correlated with serum creatinine and urinary KIM-1. Upregulated genes in CSDE1 knockout mice were enriched mianly in the PI3K–Akt signaling . The in vivo and in vitro models showed that depletion of CSDE1 activated PTEN/PI3K/Akt pathway, enhanced autophagy, inhibited apoptosis, and consequently protected the kidney.
Conclusion
CSDE1 is markedly upregulated in renal proximal tubular epithelial cells in I/R-AKI tissues, with elevated urinary CSDE1. CSDE1 knockout activates the PTEN/PI3K/Akt pathway, enhances protective autophagy, inhibits apoptosis, and protects the kidney in I/R renal injury. CSDE1 may serve as a noninvasive biomarker and therapeutic target for I/R-AKI.
AKI was alleviated in CSDE1 knockout mice