Targeting autophagy, oxidative stress, and ER stress for neurodegenerative diseases treatment

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dc.authoridAli Zarrabi / 0000-0003-0391-1769en_US
dc.authorscopusidAli Zarrabi / 23483174100
dc.authorwosidAli Zarrabi / U-2602-2019
dc.contributor.authorEsmaeili, Yasaman
dc.contributor.authorYarjanli, Zahra
dc.contributor.authorPakniya, Fatemeh
dc.contributor.authorBidram, Elham
dc.contributor.authorLos, Marek J
dc.contributor.authorEshraghi, Mehdi
dc.contributor.authorKlionsky, Daniel J
dc.contributor.authorGhavami, Saeid
dc.contributor.authorZarrabi, Ali
dc.date.accessioned2022-03-15T05:52:59Z
dc.date.available2022-03-15T05:52:59Z
dc.date.issued2022en_US
dc.departmentİstinye Üniversitesi, Mühendislik ve Doğa Bilimleri Fakültesi, Biyomedikal Mühendisliği Bölümüen_US
dc.description.abstractProtein homeostasis is a vital process for cell function and, therefore, disruption of the molecular mechanisms involved in this process, such as autophagy, may contribute to neurodegenerative diseases (NDs). Apart from autophagy disruption, excess oxidative stress and endoplasmic reticulum (ER) stress are additional main molecular mechanisms underlying neurodegeneration, leading to protein aggregation, and mitochondrial dysfunction. Notably, these primary molecular processes are interconnected pathways which have synergistic effects on each other. Therefore, we propose that targeting of the crosstalk between autophagy, oxidative stress and ER stress simultaneously may play a critical role in healing NDs. NeuroNanoTechnology, as a revolutionized approach, in combination with an in-silico strategy, holds great promise for developing de-novo structures for targeting and modulating neuro-molecular pathways. Accordingly, this review outlines the contributions of autophagy, oxidative stress, and ER stress in neurodegenerative conditions along with a particular focus on the crosstalk among these pathways. Furthermore, we provide a comprehensive discussion on the potential of nanomaterials to target this crosstalk and suggest this potential as a promising opportunity in neuroprotection.en_US
dc.identifier.citationEsmaeili Y, Yarjanli Z, Pakniya F, Bidram E, Los MJ, Eshraghi M, Klionsky DJ, Ghavami S, Zarrabi A. Targeting autophagy, oxidative stress, and ER stress for neurodegenerative diseases treatment. J Control Release. 2022 Mar 3:S0168-3659(22)00111-0. doi:en_US
dc.identifier.doi10.1016/j.jconrel.2022.03.001en_US
dc.identifier.issn0168-3659en_US
dc.identifier.pmid35248646en_US
dc.identifier.scopus2-s2.0-85126368993en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.urihttps://doi.org/10.1016/j.jconrel.2022.03.001
dc.identifier.urihttps://hdl.handle.net/20.500.12713/2550
dc.identifier.wosWOS:000783578300003en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.institutionauthorZarrabi, Ali
dc.language.isoenen_US
dc.relation.ispartofJ Control Releaseen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAutophagyen_US
dc.subjectEndoplasmic Reticulum Stressen_US
dc.subjectNanotechnologyen_US
dc.subjectNeurodegenerationen_US
dc.subjectOxidative Stressen_US
dc.titleTargeting autophagy, oxidative stress, and ER stress for neurodegenerative diseases treatmenten_US
dc.typeArticleen_US

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