Abstract: FR-PO149
Recombinant Sestrin2 Ameliorates Oxidative Stress, Mitochondrial Damage, and Renal Dysfunction in Contrast-Induced AKI
Session Information
- AKI: Mechanisms - II
November 03, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 103 AKI: Mechanisms
Author
- Oh, Hyewon, Yonsei University College of Medicine, Seodaemun-gu, Seoul, Korea (the Republic of)
Background
Although the use of iodinated contrast agents is at times essential for accurate disease diagnosis, contrast-induced acute kidney injury (CI-AKI) is a possible complication. The pathogenesis of CI-AKI has not yet been fully elucidated, but increased oxidative stress is thought to be one important cause and mitochondrial damage is thought to accompany the consequences of oxidative stress. Sestrin2 is activated by many stress factors that have been associated with oxidative stress and mitochondrial damage.
Methods
In vivo experiments, C57BL/6 mice were divided into; control, recombinant sestrin2 (RS), CI-AKI and CI-AKI with RS groups. We examined the blood analysis, oxidative stress, mitochondrial damage and CT scans.
Results
Our results showed that RS decreases oxidative stress in the CI-AKI model. Mitochondrial damage presenting as morphological changes were alleviated and ATP synthesis was restored after administration of RS. Also, the decreases in relative blood volume significantly increased compared to the CI-AKI group after RS administration in the CT scan. Finally, renal injury markers also decreased and kidney function was preserved with RS. These results suggested that RS can mitigate the deterioration of renal function in CI-AKI model.
Conclusion
Sestrin2 could mitigate mitochondrial damage and apoptosis by regulating oxidative stress in a contrast-induced acute kidney injury model.
Sestrin2 expression in the CI-AKI model
Recombinant sestrin2 attenuating renal function in the CI-AKI model
Funding
- Government Support – Non-U.S.