The protective mechanism of SIRT3 and potential therapy in acute kidney injury

Author:

Yuan Jinguo1,Zhao Jin1,Qin Yunlong12,Zhang Yumeng13,Wang Anjing13,Ma Rui4ORCID,Han Mei13,Hui Yueqing1,Guo Shuxian1,Ning Xiaoxuan4,Sun Shiren1

Affiliation:

1. Department of Nephrology, Xijing Hospital, Fourth Military Medical University , Xi’an, 710032, China

2. Department of Nephrology, 980th Hospital of PLA Joint Logistical Support Force (Bethune International Peace Hospital) , Shijiazhuang, 050011, China

3. Department of Postgraduate Student, Xi’an Medical University , Xi’an, 710021, China

4. Department of Geriatric, Xijing Hospital, Fourth Military Medical University , Xi’an, 710032, China

Abstract

Summary Acute kidney injury (AKI) is a complex clinical syndrome with a poor short-term prognosis, which increases the risk of the development of chronic kidney diseases and end-stage kidney disease. However, the underlying mechanism of AKI remains to be fully elucidated, and effective prevention and therapeutic strategies are still lacking. Given the enormous energy requirements for filtration and absorption, the kidneys are rich in mitochondria, which are unsurprisingly involved in the onset or progression of AKI. Accumulating evidence has recently documented that Sirtuin 3 (SIRT3), one of the most prominent deacetylases highly expressed in the mitochondria, exerts a protective effect on AKI. SIRT3 protects against AKI by regulating energy metabolism, inhibiting oxidative stress, suppressing inflammation, ameliorating apoptosis, inhibiting early-stage fibrosis and maintaining mitochondrial homeostasis. Besides, a number of SIRT3 activators have exhibited renoprotective properties both in animal models and in vitro experiments, but have not yet been applied to clinical practice, indicating a promising therapeutic approach. In this review, we unravel and summarize the recent advances in SIRT3 research and the potential therapy of SIRT3 activators in AKI.

Funder

National Natural Science Foundation of China

Publisher

Oxford University Press (OUP)

Subject

General Medicine

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