线粒体功能的药理调节作为治疗肠道炎症性疾病和结直肠癌的新策略。

IF 8.9
Journal of pharmaceutical analysis Pub Date : 2025-04-01 Epub Date: 2024-08-18 DOI:10.1016/j.jpha.2024.101074
Boya Wang, Xinrui Guo, Lanhui Qin, Liheng He, Jingnan Li, Xudong Jin, Dapeng Chen, Guangbo Ge
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引用次数: 0

摘要

炎症性肠病(IBD)是一种慢性和复发性肠道疾病,已成为一个主要的全球性健康问题。IBD患者患结直肠癌(CRC)的风险较高,最近的研究表明,线粒体功能障碍在IBD和CRC的发病机制中都起着关键作用。本文综述了IBD和CRC的发病机制,重点是线粒体功能障碍,并探讨了通过调节线粒体功能来解决这两种疾病的药理学靶点和策略。此外,本文还全面总结了治疗IBD和CRC的线粒体功能障碍的药理调节的最新进展,包括线粒体损伤、线粒体DNA (mtDNA)释放和线粒体自噬损伤。本文还系统介绍了天然化合物(如黄酮类化合物、生物碱和二萜)、中药和肠道微生物群通过调节线粒体功能来缓解IBD和减缓CRC进展的作用。在未来,开发更实用的方法来实时监测和准确检测线粒体功能将势在必行,这将极大地帮助科学家通过调节线粒体功能来识别更有效的治疗IBD和CRC的药物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Pharmacological modulation of mitochondrial function as novel strategies for treating intestinal inflammatory diseases and colorectal cancer.

Inflammatory bowel disease (IBD) is a chronic and recurrent intestinal disease, and has become a major global health issue. Individuals with IBD face an elevated risk of developing colorectal cancer (CRC), and recent studies have indicated that mitochondrial dysfunction plays a pivotal role in the pathogenesis of both IBD and CRC. This review covers the pathogenesis of IBD and CRC, focusing on mitochondrial dysfunction, and explores pharmacological targets and strategies for addressing both conditions by modulating mitochondrial function. Additionally, recent advancements in the pharmacological modulation of mitochondrial dysfunction for treating IBD and CRC, encompassing mitochondrial damage, release of mitochondrial DNA (mtDNA), and impairment of mitophagy, are thoroughly summarized. The review also provides a systematic overview of natural compounds (such as flavonoids, alkaloids, and diterpenoids), Chinese medicines, and intestinal microbiota, which can alleviate IBD and attenuate the progression of CRC by modulating mitochondrial function. In the future, it will be imperative to develop more practical methodologies for real-time monitoring and accurate detection of mitochondrial function, which will greatly aid scientists in identifying more effective agents for treating IBD and CRC through modulation of mitochondrial function.

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