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2015 | 2 | 1 |

Article title

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


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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.









Physical description


15 - 12 - 2014
24 - 2 - 2015
30 - 8 - 2014


  • 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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