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脓毒症:一种失败的饥饿反应。

Sepsis: a failing starvation response.

作者信息

Vandewalle Jolien, Libert Claude

机构信息

Center for Inflammation Research, Vlaams Instituut voor Biotechnologie (VIB), Ghent, Belgium; Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium.

Center for Inflammation Research, Vlaams Instituut voor Biotechnologie (VIB), Ghent, Belgium; Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium.

出版信息

Trends Endocrinol Metab. 2022 Apr;33(4):292-304. doi: 10.1016/j.tem.2022.01.006. Epub 2022 Feb 15.

Abstract

Sepsis is involved in ~ 20% of annual global deaths. Despite decades of research, the current management of sepsis remains supportive rather than curative. Clinical trials in sepsis have mainly been focused on targeting the inflammatory pathway, but without success. Recent data indicate that metabolic dysregulation takes place in sepsis, and targeting metabolic pathways might hold much promise for the management of sepsis. Sepsis yields a strong starvation response, including the release of high-energy metabolites such as lactate and free fatty acids. However, the activity of two major transcription factors, GR and PPARα, is downregulated in hepatocytes, leading to the accumulation and toxicity of metabolites that, moreover, fail to be transformed into useful molecules such as glucose and ketones. We review the literature and suggest mechanisms and potential therapeutic targets that might prevent or revert the fatal metabolic dysregulation in sepsis.

摘要

脓毒症导致全球每年约20%的死亡。尽管经过了数十年的研究,但目前脓毒症的治疗仍以支持治疗为主,而非治愈性治疗。脓毒症的临床试验主要集中在针对炎症途径,但未取得成功。最近的数据表明,脓毒症中会发生代谢失调,针对代谢途径可能为脓毒症的治疗带来很大希望。脓毒症会引发强烈的饥饿反应,包括释放高能代谢物,如乳酸和游离脂肪酸。然而,肝细胞中两种主要转录因子GR和PPARα的活性下调,导致代谢物的积累和毒性,此外,这些代谢物无法转化为有用的分子,如葡萄糖和酮。我们回顾了文献,并提出了可能预防或逆转脓毒症中致命代谢失调的机制和潜在治疗靶点。

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