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Kidney Week

Abstract: TH-PO093

Caveolin-1 Protects Against AKI via Regulating Endoplasmic Reticulum Stress

Session Information

  • AKI: Mechanisms - I
    November 02, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Zhang, Yan, Xiangya Hospital Central South University, Changsha, Hunan, China
  • Peng, Zhangzhe, Xiangya Hospital Central South University, Changsha, Hunan, China
Background

Acute renal injury (AKI) is a serious medical condition characterized by a rapid loss of renal function. Recent evidence has suggested that endoplasmic reticulum (ER) function is important for protein homeostasis (‘proteostasis’) in the kidney, and that ER stress is a component of acute kidney injury. Caveolin-1 (Cav1), a multifunctional membrane protein, is the main component of caveolae on the plasma membrane. Caveolae serve as a platform to regulate stress responses, cellular endocytosis, and signal transduction. Previous studies have shown that the expression of Cav1 was increased in AKI models induced by ischemia-reperfusion and gentamicin. However, the crucial role of Prdx1 in AKI remains unclear.

Methods

Cav1-deficient mice were used to determine its function and potential mechanisms in AKI.

Results

In ischemic-reperfusion-induced AKI mice, a significant increase in the expression of Cav1 in kidney tissue was observed. Similar observations were also obtained in the lipopolysaccharide (LPS)-induced AKI mouse model. Likely, the expression of Cav-1 was increased in patients with AKI. Cav1 deficiency worsened renal function and caused more tubular injury in AKI induced by ischemia-reperfusion and LPS. Furthermore, i.p. injection of Cav1 peptide in Cav1-/- mice improves kidney function and attenuates kidney tubular injury in ischemic-reperfusion and LPS-induced AKI mice. Additionally, knockout of Cav1 aggravated endoplasmic reticulum stress and apoptosis in primary renal tubular epithelial cells.

Conclusion

Our results revealed that Cav1 may play a protective role in AKI by regulating ER stress, thereby identifying a novel and important therapeutic target for AKI.