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Kidney Week

Abstract: FR-PO986

Empagliflozin Attenuates Renal Fibrosis Through the DsbA-L-CAS-STING Pathway in Unilateral Ureteral Obstruction Model

Session Information

  • CKD: Pathobiology - I
    November 04, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
    Abstract Time: 10:00 AM - 12:00 PM

Category: CKD (Non-Dialysis)

  • 2203 CKD (Non-Dialysis): Mechanisms

Authors

  • Cho, Junghyun, Soonchunhyang University Hospital, Seoul, Korea (the Republic of)
  • Chung, Eui Suk, Soonchunhyang University Hospital, Seoul, Korea (the Republic of)
  • Lee, Haekyung, Soonchunhyang University Hospital, Seoul, Korea (the Republic of)
  • Kwon, Soon hyo, Soonchunhyang University Hospital, Seoul, Korea (the Republic of)
Background

Chronic kidney disease (CKD) is associated with an increase in morbidity and mortality. Renal fibrosis is a common pathway leading to the progression of CKD. Recent studies have reported an improvement of CKD with use of sodium glucose cotransport 2 inhibitors (SGLT2i) in both patients with DM and those without it. However, the mechanism of SGLT2i’s effect upon CKD has not been elucidated. In current study, we examined the effect of SGLT2i on renal fibrosis in rats caused by unilateral ureteral obstruction (UUO).

Methods

Sprague Dawley rats were randomly divided into two groups (each n=8). One group was treated by Empagliflozin after UUO induction while the other group was left untreated. Kidneys were harvested two weeks after UUO. We evaluated the mitochondrial damage pathway presumed to contribute to the inflammation.

Results

UUO has resulted in marked renal fibrosis and triggered the activation of the cGAS-STING pathway. Empagliflozin has been shown to attenuate renal fibrosis and decrease the activation of the cCAS-STING pathway. The expression of disulfide-bond A oxidoreductase-like proteins (DsbA-L) was increased in the Empagliflozin group (Figure 1).

Conclusion

These findings suggest that SGLT2i attenuates the development of renal fibrosis via inhibition of mitochondrial damage.