遗传 ›› 2016, Vol. 38 ›› Issue (10): 918-927.doi: 10.16288/j.yczz.16-136
张玉娇, 李晓静, 米凯霞
收稿日期:
2016-04-19
修回日期:
2016-07-22
出版日期:
2016-10-20
发布日期:
2016-10-20
作者简介:
米凯霞,博士,副研究员,研究方向:结核分枝杆菌耐药机制。
基金资助:
Yujiao Zhang, Xiaojing Li, Kaixia Mi
Received:
2016-04-19
Revised:
2016-07-22
Online:
2016-10-20
Published:
2016-10-20
Supported by:
摘要: 结核病是由结核分枝杆菌(Mycobacterium tuberculosis)通过空气传播引起人类感染的慢性传染病,耐药结核分枝杆菌的流行是目前结核病防治的世界难题。氟喹诺酮类药物是人工合成药物,应用于耐药结核的临床治疗中,在治疗中起着核心的作用。但近年来,氟喹诺酮类药物的抗性菌株不断出现,愈发增加了结核病治疗的困难与治疗失败风险。在临床中氟喹诺酮药物的靶点比较清楚,是结核分枝杆菌的DNA旋转酶。目前发现结核分枝杆菌耐氟喹诺酮类药物的机制主要包括药物靶点DNA旋转酶的关键氨基酸改变、药物外排泵系统、细菌细胞壁厚度的增加以及喹诺酮抗性蛋白MfpA介导的DNA旋转酶活性调控。其中在氟喹诺酮靶标DNA旋转酶功能活性改变的耐药机制方面,编码DNA旋转酶基因突变一直是研究的热点,但近年来发现DNA旋转酶的调控蛋白MfpA以及DNA旋转酶的修饰在细菌耐药性中起着重要的作用,相关机制还亟待发现。本文综述了当前结核分枝杆菌耐氟喹诺酮类药物的作用机制,旨在为研发精准诊断技术和药物发掘提供科学理论基础和参考。
张玉娇, 李晓静, 米凯霞. 结核分枝杆菌耐氟喹诺酮类药物的分子机制研究进展[J]. 遗传, 2016, 38(10): 918-927.
Yujiao Zhang, Xiaojing Li, Kaixia Mi. Mechanisms of fluoroquinolone resistance in Mycobacterium tuberculosis[J]. Hereditas(Beijing), 2016, 38(10): 918-927.
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