Research progress in the pathogenesis of sepsis-associated encephalopathy

被引：3

作者：

Zhou, Yue ^{[1
]}

Bai, Lu ^{[2
]}

Tang, Wenjing ^{[3
]}

Yang, Weiying ^{[3
]}

Sun, Lichao ^{[3
]}

机构：

[1] First Hosp Jilin Univ, Teaching Dept, Changchun 130021, Peoples R China

[2] Dalian 3 Peoples Hosp, Dept Med Oncol, Dalian 116091, Peoples R China

[3] First Hosp Jilin Univ, Dept Emergency Med, Changchun 130021, Jilin, Peoples R China

来源：

HELIYON | 2024年 / 10卷 / 12期

关键词：

Sepsis; Sepsis -associated encephalopathy; Neuroinflammation; Epigenetics; Intestinal flora disorder; Hyperammonemia; NICOTINIC ACETYLCHOLINE-RECEPTOR; MICROGLIA ACTIVATION; SEPTIC SHOCK; NEUROINFLAMMATION; INJURY; ENDOTOXEMIA; PROTECTS; PATHWAY; SYSTEM; MICE;

D O I：

10.1016/j.heliyon.2024.e33458

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Sepsis is a syndrome that causes dysfunction of multiple organs due to the host 's uncontrolled response to infection and is a significant contributor to morbidity and mortality in intensive care units worldwide. Surviving patients are often left with acute brain injury and long-term cognitive impairment, known as sepsis -associated encephalopathy (SAE). In recent years, researchers have directed their focus towards the pathogenesis of SAE. However, due to the complexity of its development, there remains a lack of effective treatment measures that arise as a serious issue affecting the prognosis of sepsis patients. Further research on the possible causes of SAE aims to provide clinicians with potential therapeutic targets and help develop targeted prevention strategies. This paper aims to review recent research on the pathogenesis of SAE, in order to enhance our understanding of this syndrome.

引用

页数：13

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