The advances on autophagy the pathogenesis and treatment in septic acute kidney injury.
10.3760/cma.j.cn121430-20240904-00748
- Author:
Ziyou TIAN
1
;
Jie ZHANG
1
;
Shiqi NIE
1
;
Daihua DENG
1
;
Zhu LI
1
;
Lili TANG
2
,
3
;
Xiaoyue LI
1
Author Information
1. Department of Emergency, the Fifth Affiliated Hospital (Zhuhai) of Zunyi Medical University, Zhuhai 519100, Guangdong, China.
2. Department of Intensive Care Medicine, the Fifth Affiliated Hospital (Zhuhai) of Zunyi Medical University, Zhuhai 519100, Guangdong, China. Corresponding author: Li Xiaoyue, Email: euyeuy1983@
3. com.
- Publication Type:English Abstract
- MeSH:
Humans;
Acute Kidney Injury/etiology*;
Autophagy;
Sepsis/complications*;
Signal Transduction
- From:
Chinese Critical Care Medicine
2025;37(2):183-187
- CountryChina
- Language:Chinese
-
Abstract:
Sepsis is a life-threatening organ dysfunction syndrome caused by a dysregulated host response to infection. Septic acute kidney injury (SAKI) is one of the most common complications of sepsis, and the occurrence of acute kidney injury (AKI) indicates that the patient's condition is critical with a poor prognosis. The traditional view holds that the main mechanism of SAKI is the reduction of renal blood flow, inadequate renal perfusion, inflammatory response, and microcirculatory dysfunction caused by sepsis, which subsequently leads to ischemia and necrosis of renal tubular cells. Recent research findings indicate that processes such as autophagy and other forms of programmed cell death play an increasingly important role. Autophagy is a programmed intracellular degradation process and is a form of programmed cell death. Cells degrade their cytoplasmic components via lysosomes, breaking down and recycling intracellular constituents to meet their metabolic needs, maintain intracellular homeostasis, and renew organelles. During SAKI, autophagy plays a crucial protective role through various mechanisms, including regulating inflammation and immune responses, clearing damaged organelles, and maintaining stability in the intracellular environment. In recent years, the role of autophagy in the pathogenesis and treatment of SAKI has received widespread attention. Research has confirmed that various intracellular signaling pathways and signaling molecules targeting autophagy [such as mammalian target of rapamycin (mTOR) signaling pathway, AMP-activated protein kinase (AMPK) signaling pathway, nuclear factor-κB (NF-κB) signaling pathway, and Sirtuins (SIRT), autophagy associated factor Beclin-1, and Toll-like receptor (TLR)] are involved in the development of SAKI. Due to the complex pathogenesis of SAKI, current treatment strategies include fluid management, infection control, maintenance of internal environment balance, and renal replacement therapy; however, the mortality remains high. In recent years, it has been found that autophagy plays a critical protective role in sepsis-mediated AKI. As a result, an increasing number of drugs are being developed to alleviate SAKI by regulating autophagy. This article reviews the latest advances in the role of autophagy in the pathogenesis and treatment of SAKI, with the aim of providing insights for the development of new drugs for SAKI patients.
