DOI 10.3760/cma.j.cn121430-20250515-00474
[Research progress on the involvement of glucose transporter-mediated cerebral glucose metabolism in the regulation of sepsis-associated encephalopathy].
Аннотация
Sepsis-associated encephalopathy (SAE) refers to diffuse brain dysfunction caused by a systemic inflammatory response, in the absence of direct central nervous system infection, structural brain abnormalities, or clinical/laboratory evidence of other types of encephalopathy. It is a common complication in sepsis, and its pathogenesis has not yet been fully elucidated. Recent studies have revealed that dysregulated cerebral glucose metabolism plays an important role in the development of SAE, in which glucose transporters (GLUTs) are critically involved. This article reviews the research progress on the involvement of brain glucose metabolism mediated by GLUTs in the regulation of SAE. The study focuses on: 1) The expression and function of GLUT1, GLUT3 and GLUT4 in brain tissue. 2) The function and expression of GLUTs in brain tissue are regulated by multiple factors: estrogen, cytokines, metabolic state and mitochondrial status. 3) The mechanisms of GLUTs in SAE and related brain disorders (such as neurodegenerative diseases associated with aging, cerebral hemorrhage, meningitis, encephalopathy caused by human immunodeficiency virus infection and encephalopathy caused by burns or burns combined with infection). 4) Potential therapeutic strategies for SAE based on glucose metabolism regulation: improving the expression of GLUTs associated with blood-brain barrier function; modulating the function of GLUTs involved in neuroinflammation; enhancing mitochondrial function, reducing oxidative stress, and increasing adenosine triphosphate production to indirectly boost GLUTs expression and activity; metabolic reprogramming-adjusting key metabolic enzymes or pathways to alter cellular metabolic characteristics and adapt to the energy demands during sepsis. The aim is to provide a theoretical basis for a deeper understanding of the pathophysiological mechanisms of SAE and the development of new therapeutic targets.
Предметные рубрики MeSH
Подготовка и перевод публикации
Обработка статьи · этапы, ошибки и управление
Ошибки и ограничения
История · было → стало
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