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揭开葡萄糖代谢重编程的秘密:其在肺部疾病中的作用。

Unlocking the secrets of glucose metabolism reprogramming: the role in pulmonary diseases.

作者信息

Li Zhen, Chen Shuo-Xuan, Jiang Shuai, Yang Yi-Nong, Yan Xi-Chan

机构信息

School of Basic Medical Sciences, Hunan University of Medicine, Huaihua, Hunan, China.

School of Rehabilitation Medicine and Health, Hunan University of Medicine, Huaihua, Hunan, China.

出版信息

Front Pharmacol. 2025 Aug 13;16:1551452. doi: 10.3389/fphar.2025.1551452. eCollection 2025.

DOI:10.3389/fphar.2025.1551452
PMID:40880642
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12380867/
Abstract

Metabolic reprogramming is the process by which cells adapt to different patterns of energy metabolism in response to the demands of the microenvironment for energy and biological macromolecules. Glucose serves as the primary energy source for cellular survival, and its metabolic pathways are intricately associated with cellular functional states. Recent studies have demonstrated that alterations in glucose metabolism, along with non-metabolic functions of metabolic enzymes and metabolites, play crucial roles in the development and progression of lung diseases under inflammatory conditions. This review summarizes the regulatory mechanisms of glucose metabolism across various pulmonary disorders and discusses the non-metabolic functions of glycolytic enzymes and metabolites in relation to disease pathogenesis. We aim to shine new light on the diagnosis and treatment of lung disease.

摘要

代谢重编程是细胞根据微环境对能量和生物大分子的需求,适应不同能量代谢模式的过程。葡萄糖是细胞生存的主要能量来源,其代谢途径与细胞功能状态密切相关。最近的研究表明,葡萄糖代谢的改变以及代谢酶和代谢产物的非代谢功能,在炎症条件下肺部疾病的发生和发展中起着关键作用。本综述总结了各种肺部疾病中葡萄糖代谢的调节机制,并讨论了糖酵解酶和代谢产物的非代谢功能与疾病发病机制的关系。我们旨在为肺部疾病的诊断和治疗提供新的思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34ef/12380867/2082710f4407/fphar-16-1551452-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34ef/12380867/1fb54b623bcc/fphar-16-1551452-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34ef/12380867/d5c9493cf840/fphar-16-1551452-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34ef/12380867/601d4fb58264/fphar-16-1551452-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34ef/12380867/2082710f4407/fphar-16-1551452-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34ef/12380867/1fb54b623bcc/fphar-16-1551452-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34ef/12380867/d5c9493cf840/fphar-16-1551452-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34ef/12380867/601d4fb58264/fphar-16-1551452-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34ef/12380867/2082710f4407/fphar-16-1551452-g004.jpg

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本文引用的文献

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Circ0515 reprogramming mitochondrial succinate metabolism and promotes lung adenocarcinoma progression through regulating SDHB.Circ0515 通过调节 SDHB 重编程线粒体琥珀酸代谢并促进肺腺癌进展。
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Targeting the STAT3/ACLY axis attenuates pulmonary inflammation but delays Mycoplasma pneumoniae clearance via citrate metabolism.靶向 STAT3/ACLY 轴可减轻肺部炎症,但通过柠檬酸代谢会延迟肺炎支原体的清除。
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Tobacco Smoking Rewires Cell Metabolism by Inducing GAPDH Succinylation to Promote Lung Cancer Progression.吸烟通过诱导甘油醛-3-磷酸脱氢酶琥珀酰化来重塑细胞代谢,从而促进肺癌进展。
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Palmitoylated COX-2 reprogrammed mitochondrial metabolism in pyroptotic inflammatory injury in patients with post-acute COVID-19 syndrome.棕榈酰化的COX-2在急性后COVID-19综合征患者的焦亡性炎症损伤中重编程线粒体代谢。
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Gut flora-derived succinate exacerbates Allergic Airway Inflammation by promoting protein succinylation.肠道菌群衍生的琥珀酸通过促进蛋白质琥珀酰化加剧过敏性气道炎症。
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Study on the mechanism of Jieduquyuziyin prescription improving the condition of MRL/lpr mice by regulating T cell metabolic reprogramming through the AMPK/mTOR pathway.解毒祛瘀滋阴方通过AMPK/mTOR途径调节T细胞代谢重编程改善MRL/lpr小鼠病情的机制研究
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MOTS-c Promotes Glycolysis via AMPK-HIF-1α-PFKFB3 Pathway to Ameliorate CPB-induced Lung Injury.心肌代谢物-胱抑素C通过AMPK-HIF-1α-PFKFB3途径促进糖酵解以改善体外循环诱导的肺损伤。
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