Melatonin: a promising neuroprotective agent for cerebral ischemia-reperfusion injury

Basit Öğe Kaydı
dc.authorscopusid56003654100
dc.authorscopusid57216431373
dc.authorscopusid56108184000
dc.authorscopusid57212299393
dc.authorscopusid55565668500
dc.authorscopusid57977733500
dc.contributor.authorTozihi, Majid
dc.contributor.authorShademan, Behrouz
dc.contributor.authorYousefi, Hadi
dc.contributor.authorBiray Avcı, Çığır
dc.contributor.authorNourazarian, Alireza
dc.contributor.authorDehghan, Gholamreza
dc.date.accessioned2024-08-25T18:47:33Z
dc.date.available2024-08-25T18:47:33Z
dc.date.issued2023
dc.departmentEge Üniversitesien_US
dc.description.abstractCerebral ischemia-reperfusion (CIR) injury is initiated by the generation of reactive oxygen species (ROS), which leads to the oxidation of cellular proteins, DNA, and lipids as an initial event. The reperfusion process impairs critical cascades that support cell survival, including mitochondrial biogenesis and antioxidant enzyme activity. Failure to activate prosurvival signals may result in increased neuronal cell death and exacerbation of CIR damage. Melatonin, a hormone produced naturally in the body, has high concentrations in both the cerebrospinal fluid and the brain. However, melatonin production declines significantly with age, which may contribute to the development of age-related neurological disorders due to reduced levels. By activating various signaling pathways, melatonin can affect multiple aspects of human health due to its diverse range of activities. Therefore, understanding the underlying intracellular and molecular mechanisms is crucial before investigating the neuroprotective effects of melatonin in cerebral ischemia-reperfusion injury.en_US
dc.identifier.doi10.3389/fnagi.2023.1227513
dc.identifier.issn1663-4365
dc.identifier.pmid37600520en_US
dc.identifier.scopus2-s2.0-85168358879en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.urihttps://doi.org/10.3389/fnagi.2023.1227513
dc.identifier.urihttps://hdl.handle.net/11454/101962
dc.identifier.volume15en_US
dc.identifier.wosWOS:001050179200001en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherFrontiers Media Saen_US
dc.relation.ispartofFrontiers In Aging Neuroscienceen_US
dc.relation.publicationcategoryDiğeren_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.snmz20240825_Gen_US
dc.subjectmelatoninen_US
dc.subjectcerebral ischemia-reperfusion injuryen_US
dc.subjectreactive oxygen species (ROS)en_US
dc.subjectischemic strokesen_US
dc.subjectneuroprotective agenten_US
dc.subjectEndoplasmic-Reticulum Stressen_US
dc.subjectCentral-Nervous-Systemen_US
dc.subjectIschemia/Reperfusion Injuryen_US
dc.subjectSignaling Pathwayen_US
dc.subjectCell-Deathen_US
dc.subjectMicrovascular Obstructionen_US
dc.subjectMyocardial-Infarctionen_US
dc.subjectTranscription Factoren_US
dc.subjectProtects Brainen_US
dc.subjectAutophagyen_US
dc.titleMelatonin: a promising neuroprotective agent for cerebral ischemia-reperfusion injuryen_US
dc.typeReview Articleen_US

Dosyalar

Koleksiyon

WoS İndeksli Yayınlar Koleksiyonu
PubMed İndeksli Yayın Koleksiyonu
Scopus İndeksli Yayınlar Koleksiyonu