Publication:
Basic mechanisms in endoplasmic reticulum stress and relation to cardiovascular diseases

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dc.contributor.authorSÖZEN, AHMET ERDİ
dc.contributor.authorsSozen, Erdi; Karademir, Betul; Ozer, Nesrin Kartal
dc.date.accessioned2022-03-10T15:25:16Z
dc.date.available2022-03-10T15:25:16Z
dc.date.issued2015
dc.description.abstractThe folding process is an important step in protein synthesis for the functional shape or conformation of the protein. The endoplasmic reticulum (ER) is the main organelle for the correct folding procedure, which maintains the homeostasis of the organism. This process is normally well organized under unstressed conditions, whereas it may fail under oxidative and ER stress. The unfolded protein response (UPR) is a defense mechanism that removes the unfolded/misfolded proteins to prevent their accumulation, and two main degradation systems are involved in this defense, including the proteasome and autophagy. Cells decide which mechanism to use according to the type, severity, and duration of the stress. If the stress is too severe and in excess, the capacity of these degradation mechanisms, proteasomal degradation and autophagy, is not sufficient and the cell switches to apoptotic death. Because the accumulation of the improperly folded proteins leads to several diseases, it is important for the body to maintain this balance. Cardiovascular diseases are one of the important disorders related to failure of the UPR. Especially, protection mechanisms and the transition to apoptotic pathways have crucial roles in cardiac failure and should be highlighted in detailed studies to understand the mechanisms involved. This review is focused on the involvement of the proteasome, autophagy, and apoptosis in the UPR and the roles of these pathways in cardiovascular diseases. (C) 2014 Elsevier Inc. All rights reserved.
dc.identifier.doi10.1016/j.freeradbiomed.2014.09.031
dc.identifier.eissn1873-4596
dc.identifier.issn0891-5849
dc.identifier.pubmed25452144
dc.identifier.urihttps://hdl.handle.net/11424/220181
dc.identifier.wosWOS:000348178700004
dc.language.isoeng
dc.publisherELSEVIER SCIENCE INC
dc.relation.ispartofFREE RADICAL BIOLOGY AND MEDICINE
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectEndoplasmic reticulum stress
dc.subjectProteasome
dc.subjectAutophagy
dc.subjectApoptosis
dc.subjectCardiovascular diseases
dc.subjectFree radicals
dc.subjectUNFOLDED-PROTEIN RESPONSE
dc.subjectACTIVATING TRANSCRIPTION FACTOR-6
dc.subjectATTENUATES CARDIOMYOCYTE DEATH
dc.subjectUBIQUITIN-PROTEASOME SYSTEM
dc.subjectCARDIAC MYOCYTE APOPTOSIS
dc.subjectPANCREATIC BETA-CELL
dc.subjectER STRESS
dc.subjectQUALITY-CONTROL
dc.subjectOXIDATIVE STRESS
dc.subjectMESSENGER-RNA
dc.titleBasic mechanisms in endoplasmic reticulum stress and relation to cardiovascular diseases
dc.typereview
dspace.entity.typePublication
local.avesis.id55dfa3c4-4acc-4677-80a4-645a8c06a8d8
local.import.packageSS5
local.indexed.atWOS
local.indexed.atSCOPUS
local.indexed.atPUBMED
local.journal.numberofpages12
oaire.citation.endPage41
oaire.citation.startPage30
oaire.citation.titleFREE RADICAL BIOLOGY AND MEDICINE
oaire.citation.volume78
relation.isAuthorOfPublication47991a21-cce9-4b87-b091-bede64f8b4e0
relation.isAuthorOfPublication.latestForDiscovery47991a21-cce9-4b87-b091-bede64f8b4e0

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