Research advances in mitochondrial dysfunction-mediated sepsis-associated encephalopathy.
10.3760/cma.j.cn121430-20250213-00126
- Author:
Xueling ZHANG
1
;
Yaxuan ZHANG
;
Bin ZHANG
;
Guangzhi SHI
Author Information
1. Department of Critical Care Medicine, Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China. Corresponding author: Shi Guangzhi, Email: shigzh@aliyun.com.
- Publication Type:English Abstract
- MeSH:
Humans;
Sepsis-Associated Encephalopathy/metabolism*;
Mitochondria/metabolism*;
Sepsis/complications*;
Oxidative Stress;
Cognitive Dysfunction;
Autophagy
- From:
Chinese Critical Care Medicine
2025;37(9):885-888
- CountryChina
- Language:Chinese
-
Abstract:
Sepsis-associated encephalopathy (SAE) is one of the complications of sepsis, causes cognitive dysfunction ranging from mild attention deficits to progression into coma, which severely impairs patients' ability to live and mental health, and increases the long-term disability and mortality rates. Although the clinical attention to SAE has been increasing in recent years, effective interventions to improve cognitive dysfunction in sepsis survivors are still in the preclinical stage. The pathogenesis of SAE is numerous and complex, and mitochondrial dysfunction, as one of the key pathogenic mechanisms, plays a role in the cognitive development process through oxidative stress imbalance, energy metabolism disorders, and activation of apoptosis signaling pathway. The present review systematically integrates the recent studies on mitochondrial dysfunction in the development of cognitive disorders. This review systematically integrates the cutting-edge research results in recent years, discusses the mitochondrial structural disruption, mitochondrial kinetic abnormalities, respiratory chain dysfunction, and comprehensively comprehends the research progress of mitochondria-targeted antioxidant, mitochondrial autophagy activator, mitochondrial biosynthesis modifier and other novel intervention strategies in improving cognitive function of SAE patients, with the aim of providing theoretical basis for the breakthrough of the current status of clinical treatment of SAE and the targeting of mitochondria for treatment. The aim is to provide theoretical basis for breaking through the status of SAE clinical treatment and targeting mitochondrial therapy.
