非甾体抗炎药对巷道内质网应激反应的影响

IF 0.7
Fernanda L. B. Mügge, Aristóbolo Mendes Silva
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引用次数: 6

摘要

在过去的十年中,有少量证据表明非甾体抗炎药(NSAIDs)对内质网(ER)的稳态有影响。它们进入细胞最终将导致介导内质网应激反应的关键分子的激活或抑制,这不仅引起了人们对内质网应激反应的药理学靶点的兴趣,而且引起了由非甾体抗炎药诱导的内质网应激介导效应如何在治疗上有利或不利的重要问题。我们在此综述非甾体抗炎药的毒性作用和治疗应用,涉及三个主要内质网应激臂,即PERK, IRE1和ATF6。首先,我们简要介绍了这些内质网应激因子介导的下游事件,然后介绍了非甾体抗炎药化合物和作用方式,最后介绍了它们对内质网应激反应的影响。非甾体抗炎药是一种很有前途的药物,针对癌症和其他疾病的不同方面的内质网应激成分,但更好地理解其益处和危害的机制,必将为几种疾病的治疗铺平道路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Endoplasmic reticulum stress response in the roadway for the effects of non-steroidal anti-inflammatory drugs
Abstract Over the past decade, a handful of evidence has been provided that nonsteroidal anti-inflammatory drugs (NSAIDs) display effects on the homeostasis of the endoplasmic reticulum (ER). Their uptake into cells will eventually lead to activation or inhibition of key molecules that mediate ER stress responses, raising not only a growing interest for a pharmacological target in ER stress responses but also important questions how the ER-stress mediated effects induced by NSAIDs could be therapeutically advantageous or not. We review here the toxicity effects and therapeutic applications of NSAIDs involving the three majors ER stress arms namely PERK, IRE1, and ATF6. First, we provide brief introduction on the well-established and characterized downstream events mediated by these ER stress players, followed by presentation of the NSAIDs compounds and mode of action, and finally their effects on ER stress response. NSAIDs present promising drug agents targeting the components of ER stress in different aspects of cancer and other diseases, but a better comprehension of the mechanisms underlying their benefits and harms will certainly pave the road for several diseases’ therapy.
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