溢出系统在整个生物领域推动了耐药性和毒性
Pedro Eduardo Almeida da Silva1, Andrea Von Groll1, Ivy Ramis1
1Universidade Federal do Rio Grande, Rio Grande, RS, Brazil.
PeerJ
|December 1, 2025
概括
溢出驱动病原体和癌症的多药性耐药性和毒性. 开发排泄抑制剂面临挑战,但像CRISPR这样的新技术为克服阻力提供了希望.
科学领域:
- 微生物学 微生物学
- 生物化学 生物化学
- 药理学 药理学是指药理学的学科.
背景情况:
- 排泄 (EP) 是膜蛋白,对细菌,真菌和癌细胞的多药性抵抗 (MDR) 至关重要.
- 这些积极排出治疗剂,降低药物的疗效,并导致治疗失败.
- EPs还在毒性,生物膜形成,免疫逃避和持久性方面发挥作用.
研究的目的:
- 综合出流在抗微生物和抗瘤耐药性的作用.
- 审查EP对不同生物领域的毒性和持久性的贡献.
- 批判性地评估当前和新兴的检测和抑制排泄的策略.
主要方法:
- 在PubMed,Scopus和Web of Science中使用结构化搜索进行了叙事审查.
- 关键词包括流出系统,抵抗机制,毒性因子,检测方法和抑制剂.
- 结合了体外,体内和临床研究的数据,以及新兴技术,如CRISPR,生物传感器和微流体.
主要成果:
- 来自RND,ABC和MFS等家族的排泄在病原体 (例如大肠杆菌,P. aeruginosa) 和癌细胞中介导MDR.
- EPs调节生物膜的形成,毒性因子的分泌和代谢适应.
- 传统的检测方法有局限性;新技术提供了更高的精度. 临床前的EPI显示出有希望的结果,但面临临临床翻译障碍.
结论:
- 溢出系统是药物耐药性和病原性的核心.
- 开发有效的排泄抑制剂 (EPI) 是一个挑战,但检测,基因编辑 (CRISPR) 和药物设计方面的进步具有潜力.
- 了解排泄动态对于开发辅助疗法来对抗MDR至关重要.
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