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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.

DOI:10.1016/j.tem.2022.01.006
PMID:35181202
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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1
Sepsis: a failing starvation response.脓毒症:一种失败的饥饿反应。
Trends Endocrinol Metab. 2022 Apr;33(4):292-304. doi: 10.1016/j.tem.2022.01.006. Epub 2022 Feb 15.
2
Hepatic PPARα function and lipid metabolic pathways are dysregulated in polymicrobial sepsis.多微生物脓毒症中肝 PPARα 功能和脂质代谢途径失调。
EMBO Mol Med. 2020 Feb 7;12(2):e11319. doi: 10.15252/emmm.201911319. Epub 2020 Jan 9.
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Hepatic PPARα is critical in the metabolic adaptation to sepsis.肝组织过氧化物酶体增殖物激活受体-α(PPARα)在脓毒症代谢适应中起关键作用。
J Hepatol. 2019 May;70(5):963-973. doi: 10.1016/j.jhep.2018.12.037. Epub 2019 Jan 21.
4
Role of the liver in regulation of ketone body production during sepsis.肝脏在脓毒症期间酮体生成调节中的作用。
J Clin Invest. 1979 Dec;64(6):1565-72. doi: 10.1172/JCI109617.
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Sepsis Care Pathway 2019.2019年脓毒症护理路径
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Activities of enzymes of fat and ketone-body metabolism and effects of starvation on blood concentrations of glucose and fat fuels in teleost and elasmobranch fish.硬骨鱼和软骨鱼脂肪及酮体代谢酶的活性以及饥饿对其血液中葡萄糖和脂肪燃料浓度的影响。
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Short-chain fatty acids and ketones directly regulate sympathetic nervous system via G protein-coupled receptor 41 (GPR41).短链脂肪酸和酮体通过 G 蛋白偶联受体 41(GPR41)直接调节交感神经系统。
Proc Natl Acad Sci U S A. 2011 May 10;108(19):8030-5. doi: 10.1073/pnas.1016088108. Epub 2011 Apr 25.

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HNF4α contributes to hepatic CAR dysfunction in polymicrobial sepsis.肝细胞核因子4α(HNF4α)在多重微生物败血症中导致肝脏组成型雄烷受体(CAR)功能障碍。
Front Immunol. 2025 Aug 19;16:1625104. doi: 10.3389/fimmu.2025.1625104. eCollection 2025.
2
Transcriptomic Profiling Reveals Distinct Immune Dysregulation in Early-Stage Sepsis Patients.转录组分析揭示早期脓毒症患者存在明显的免疫失调
Int J Mol Sci. 2025 Jul 11;26(14):6647. doi: 10.3390/ijms26146647.
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Review of research progress in sepsis-associated acute kidney injury.脓毒症相关性急性肾损伤的研究进展综述
Front Mol Biosci. 2025 Jul 11;12:1603392. doi: 10.3389/fmolb.2025.1603392. eCollection 2025.
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High-altitude adaptation as a protective factor against postoperative pulmonary complications in liver resection: a prospective matched cohort study.高原适应作为肝切除术后肺部并发症的保护因素:一项前瞻性配对队列研究。
BMC Anesthesiol. 2025 Jul 17;25(1):352. doi: 10.1186/s12871-025-03215-7.
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Acidosis Licenses the NLRP3 Inflammasome-Inhibiting Effects of Beta-Hydroxybutyrate and Short-Chain Carboxylic Acids.酸中毒使β-羟基丁酸酯和短链羧酸具有抑制NLRP3炎性小体的作用。
bioRxiv. 2025 May 7:2025.05.01.650510. doi: 10.1101/2025.05.01.650510.
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The association between stress hyperglycemia and poor outcome in critically ill children is modulated by hyperlactatemia.危重症儿童应激性高血糖与不良预后之间的关联受高乳酸血症调节。
Front Endocrinol (Lausanne). 2025 Jun 18;16:1518746. doi: 10.3389/fendo.2025.1518746. eCollection 2025.
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Modulatory role of radioprotective 105 in mitigating oxidative stress and ferroptosis via the HO-1/SLC7A11/GPX4 axis in sepsis-mediated renal injury.辐射防护蛋白105通过HO-1/SLC7A11/GPX4轴在脓毒症介导的肾损伤中减轻氧化应激和铁死亡的调节作用
Cell Death Discov. 2025 Jul 1;11(1):290. doi: 10.1038/s41420-025-02578-7.
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Research progress in the regulatory mechanism of silent information regulator 1 in sepsis (Review).沉默信息调节因子1在脓毒症中调节机制的研究进展(综述)
Mol Med Rep. 2025 Aug;32(2). doi: 10.3892/mmr.2025.13573. Epub 2025 May 26.
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Multi-Omics and -Organ Insights into Energy Metabolic Adaptations in Early Sepsis Onset.多组学和多器官对脓毒症早期发作时能量代谢适应性的见解
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Fatty acid synthesis promotes mtDNA release via ETS1-mediated oligomerization of VDAC1 facilitating endothelial dysfunction in sepsis-induced lung injury.脂肪酸合成通过ETS1介导的VDAC1寡聚促进线粒体DNA释放,从而加剧脓毒症诱导的肺损伤中的内皮功能障碍。
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