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脓毒症驱动的代谢重编程塑造了癌症免疫治疗疗效、转移潜能和药物敏感性。

Sepsis-driven metabolic reprogramming shapes cancer immunotherapy efficacy, metastatic potential, and drug sensitivity.

作者信息

Wang Leyi, Wu Changdong, Hou Ming, Li Zhiwei

机构信息

People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi, China.

Clinical Laboratory Center, People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi, China.

出版信息

Front Immunol. 2025 Sep 1;16:1642477. doi: 10.3389/fimmu.2025.1642477. eCollection 2025.

DOI:10.3389/fimmu.2025.1642477
PMID:40959054
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12433976/
Abstract

Sepsis and cancer interact in a complex, bidirectional manner that significantly impacts patient prognosis, with metabolic reprogramming being a key factor. Sepsis-induced immune dysregulation and metabolic changes promote immunosuppression, tumor growth, metastasis, and resistance to immunotherapy. Cancer patients, especially those on immunosuppressive therapies, are more vulnerable to sepsis, complicating treatment and worsening outcomes. An integrated approach combining immunotherapy, metabolic interventions, and antimicrobial strategies is essential, alongside identifying biomarkers for personalized care. Recent advancements emphasize the need to integrate molecular insights, immunotherapy, and drug sensitivity analysis. This review explores how sepsis-driven metabolic reprogramming affects cancer immunotherapy and metastasis, providing a foundation for future integrated treatment strategies. Further research should focus on developing precise therapies that regulate metabolism, immunity, and the microbiome.

摘要

脓毒症与癌症以复杂的双向方式相互作用,这对患者预后有重大影响,其中代谢重编程是一个关键因素。脓毒症诱导的免疫失调和代谢变化会促进免疫抑制、肿瘤生长、转移以及对免疫治疗的抗性。癌症患者,尤其是那些接受免疫抑制治疗的患者,更容易发生脓毒症,使治疗复杂化并恶化预后。将免疫治疗、代谢干预和抗菌策略相结合的综合方法至关重要,同时还需确定用于个性化治疗的生物标志物。最近的进展强调了整合分子见解、免疫治疗和药物敏感性分析的必要性。本综述探讨了脓毒症驱动的代谢重编程如何影响癌症免疫治疗和转移,为未来的综合治疗策略奠定基础。进一步的研究应专注于开发调节代谢、免疫和微生物群的精确疗法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d59/12433976/d0008206216a/fimmu-16-1642477-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d59/12433976/4ebd3ac0d641/fimmu-16-1642477-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d59/12433976/d0008206216a/fimmu-16-1642477-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d59/12433976/4ebd3ac0d641/fimmu-16-1642477-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d59/12433976/d0008206216a/fimmu-16-1642477-g002.jpg

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本文引用的文献

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Characterisation of an autochthonous mouse ccRCC model of immune checkpoint inhibitor therapy resistance.一种免疫检查点抑制剂治疗耐药的自发性小鼠肾透明细胞癌模型的表征
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Continuous expression of TOX safeguards exhausted CD8 T cell epigenetic fate.TOX的持续表达保障了耗竭性CD8 T细胞的表观遗传命运。
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Exploring the role of adipokines in exercise-induced inhibition of tumor growth.探索脂肪因子在运动诱导的肿瘤生长抑制中的作用。
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The Vascular Endothelial Growth Factor-A121/Vascular Endothelial Growth Factor-A165 Ratio as a Predictor of the Therapeutic Response to Immune Checkpoint Inhibitors in Gastric Cancer.血管内皮生长因子-A121/血管内皮生长因子-A165比值作为胃癌免疫检查点抑制剂治疗反应的预测指标
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BMC Cancer. 2024 Oct 7;24(1):1233. doi: 10.1186/s12885-024-13003-0.
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From immune dysregulation to organ dysfunction: understanding the enigma of Sepsis.从免疫失调到器官功能障碍:解读脓毒症之谜。
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