Sepsis-associated encephalopathy: Autophagy and miRNAs regulate microglial activation

• Published in: Physiological reports Vol. 12; no. 5; p. e15964
• Main Authors: Qin, Nannan, Miao, Yanmei, Xie, Leiyu, Ma, Xinglong, Xie, Peng
• Format: Journal Article
• Language: English
• Published: United States John Wiley & Sons, Inc 01.03.2024; John Wiley and Sons Inc; Wiley
• Subjects: Alzheimer's disease; Apoptosis; Autophagy; Brain damage; Cell death; Central nervous system; Central nervous system diseases; Chemokines; Cytokines; Disease; Encephalopathy; Homeostasis; Humans; Infections; Inflammation; Intensive care; Macrophages; Medical prognosis; Metabolism; Microglia; microRNA; MicroRNAs - genetics; miRNA; Mortality; Nervous system; neuroinflammation; Neurological complications; Neurological disorders; Neuropathology; Oxidation; Oxidative stress; Pathogenesis; Pathogens; Phenotypes; Physiology; Proteins; Review; Reviews; Sepsis; Sepsis - complications; Sepsis-Associated Encephalopathy; Therapeutic targets; microRNA; sepsis-associated encephalopathy; autophagy; neuroinflammation; microglia
• ISSN: 2051-817X
• DOI: 10.14814/phy2.15964

Sepsis-associated encephalopathy (SAE) describes diffuse or multifocal cerebral dysfunction caused by the systemic inflammatory response to sepsis. SAE is a common neurological complication in patients in the middle and late stages of sepsis in the intensive care unit. Microglia, resident macrophages of the central nervous system, phagocytose small numbers of neuronal cells and apoptotic cells, among other cells, to maintain the dynamic balance of the brain's internal environment. The neuroinflammatory response induced by activated microglia plays a central role in the pathogenesis of various central nervous system diseases. In this paper, we systematically describe the functions and phenotypes of microglia, summarize how microglia mediate neuroinflammation and contribute to the occurrence and development of SAE, and discuss recent progress in autophagy- and microRNA-mediated regulation of microglial activation to provide a theoretical basis for the prevention and treatment of SAE and identify related therapeutic targets.