Abstract: FR-PO0178
Proximal Tubule-Specific Protein ACSM2 Facilitates Recovery from AKI
Session Information
- AKI: Mechanisms - 2
November 07, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 103 AKI: Mechanisms
Authors
- Watanabe, Hirofumi, Division of Clinical Nephrology and Rheumatology, Kidney Research Center, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
- Shiiya, Takamitsu, Division of Clinical Nephrology and Rheumatology, Kidney Research Center, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
- Aida, Ryo, Division of Clinical Nephrology and Rheumatology, Kidney Research Center, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
- Sakurazawa, Chihiro, Division of Clinical Nephrology and Rheumatology, Kidney Research Center, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
- Goto, Shin, Division of Clinical Nephrology and Rheumatology, Kidney Research Center, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
- Sequeira Lopez, Maria Luisa S., Department of Pediatrics, Child Health Research Center, University of Virginia School of Medicine, Charlottesville, Virginia, United States
- Gomez, Roberto Ariel, Department of Pediatrics, Child Health Research Center, University of Virginia School of Medicine, Charlottesville, Virginia, United States
- Yamamoto, Suguru, Division of Clinical Nephrology and Rheumatology, Kidney Research Center, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
Background
Acyl-coenzyme A synthetase medium-chain family member 2 (ACSM2) has recently been identified as a protein specifically expressed in renal proximal tubules. ACSM2 is potentially involved in lipid metabolism and has been shown to correlate with renal function and the maturation status of proximal tubular cells. However, its exact biological functions and its role in kidney injury remain unclear.
Methods
To characterize temporal changes following acute kidney injury (AKI), wild-type C57BL/6 mice received a single intraperitoneal injection of folic acid, and subsequent renal injury and Acsm2 gene expression were monitored at multiple time points. Additionally, Acsm2 gene knockout mice were used to determine how the absence of Acsm2 affects the severity of folic acid-induced AKI and the renal recovery process from AKI compared to controls.
Results
Following folic acid-induced AKI, Acsm2 gene expression significantly decreased, reaching its lowest level at day 3, and showed a tendency to recover by day 14. This temporal pattern of Acsm2 expression was inversely correlated with kidney injury markers, including KIM1, NGAL, and collagen type I. At baseline conditions, Acsm2 knockout mice exhibited no signs of renal dysfunction. Moreover, there were no significant differences in the severity of renal injury between knockout and control mice at 24 hours after folic acid administration. However, at day 14 post-injection, Acsm2 knockout mice displayed significantly elevated blood urea nitrogen levels and increased renal expression of injury markers, along with more severe histological damage in tubular and interstitial compartments compared to controls.
Conclusion
Acsm2 expression dynamically changes during the course of AKI and recovery. These findings suggest that Acsm2 may play a critical role in promoting renal recovery following acute kidney injury.
Funding
- Private Foundation Support