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Tytuł artykułu

Endoplasmic reticulum stress response in the roadway for the effects of non-steroidal anti-inflammatory drugs

Treść / Zawartość
Warianty tytułu
Języki publikacji
EN
Abstrakty
EN
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.
Słowa kluczowe
EN
NSAIDs   PERK   IRE1   ATF6   CHOP   GRP78   XBP1   cancer cells  
Wydawca

Rocznik
Tom
2
Numer
1
Opis fizyczny
Daty
otrzymano
2014-08-30
zaakceptowano
2014-12-15
online
2015-02-24
Twórcy
  • Laboratory of Inflammatory Genes, Institute
    of Biological Sciences, Federal University of Minas Gerais, Belo
    Horizonte, MG, Brazil
  • Laboratory of
    Inflammatory Genes, Institute of Biological Sciences, Federal
    University of Minas Gerais – Av. Antonio Carlos, 6627 – UFMG,
    ICB, Rm J3-243. CEP: 31270-901 Belo Horizonte, MG, Brazil
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Typ dokumentu
Bibliografia
Identyfikatory
Identyfikator YADDA
bwmeta1.element.-psjd-doi-10_1515_ersc-2015-0001
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