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dc.contributor.authorPaskeh, Mahshid Deldar Abad
dc.contributor.authorAsadi, Ava
dc.contributor.authorMirzaei, Sepideh
dc.contributor.authorHashemi, Mehrdad
dc.contributor.authorEntezari, Maliheh
dc.contributor.authorRaesi, Rasoul
dc.contributor.authorHushmandi, Kiavash
dc.contributor.authorZarrabi, Ali
dc.contributor.authorErtas, Yavuz Nuri
dc.contributor.authorAref, Amir Reza
dc.contributor.authorSamarghandian, Saeed
dc.contributor.authorReiter, Russel J
dc.contributor.authorRen, Jun
dc.date.accessioned2022-04-06T05:47:24Z
dc.date.available2022-04-06T05:47:24Z
dc.date.issued2022en_US
dc.identifier.citationPaskeh, M. D. A., Asadi, A., Mirzaei, S., Hashemi, M., Entezari, M., Raesi, R., ... & Ren, J. (2022). Targeting AMPK signaling in ischemic/reperfusion injury: From molecular mechanism to pharmacological interventions. Cellular Signalling, 110323.en_US
dc.identifier.urihttps://doi.org/10.1016/j.cellsig.2022.110323
dc.identifier.urihttps://hdl.handle.net/20.500.12713/2621
dc.description.abstractIschemia is a pathological process in which blood supply to a particular organ is temporarily interrupted resulting in disturbed biological function and homeostasis of local tissues. Following ischemia, reperfusion and reoxygenation may occur which further worsens oxidative stress-mediated damage in cells and tissues. The combined processes are referred to as ischemia/reperfusion (I/R) injury. Immediate management and treatment of I/R is of utmost importance for preventing irreversible and extensive cellular damage. Apoptosis, inflammation and oxidative stress are the most validated pathologies associated with I/R. AMP-activated protein kinase (AMPK) modulates energy metabolism in cells and its activation occurs in response to elevated AMP and ADP levels. Aberrant levels of AMPK are noted in various pathological settings such as diabetes mellitus, cancer and neurological diseases. This review emphasizes AMPK signaling, its related molecular pathways and therapeutic utility during I/R. Activation of AMPK through phosphorylation prevents apoptosis and reduces oxidative stress and inflammation upon I/R. Inducing AMPK signaling normalizes mitochondrial function to inhibit cell death. Autophagy as a cytoprotective mechanism undergoes activation by AMPK/mTOR and AMPK/ULK1 pathways. AMPK reinforces the antioxidant defense capacity via Nrf2 signaling to counteract oxidative stress in I/R. Protective compounds including phytochemicals activate AMPK to alleviate I/R injury.en_US
dc.language.isoenen_US
dc.relation.ispartofCell Signalen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAMPKen_US
dc.subjectApoptosisen_US
dc.subjectAutophagyen_US
dc.subjectCell Deathen_US
dc.subjectIschemia/Reperfusion Injuryen_US
dc.subjectOxidative Stressen_US
dc.titleTargeting AMPK signaling in ischemic/reperfusion injury: From molecular mechanism to pharmacological interventionsen_US
dc.typeArticleen_US
dc.departmentİstinye Üniversitesi, Mühendislik ve Doğa Bilimleri Fakültesi, Biyomedikal Mühendisliği Bölümüen_US
dc.authoridAli Zarrabi / 0000-0003-0391-1769en_US
dc.institutionauthorZarrabi, Ali
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.identifier.pmid35358642en_US
dc.identifier.wosWOS:000799587100003en_US
dc.authorwosidAli Zarrabi / U-2602-2019
dc.authorscopusidAli Zarrabi / 23483174100
dc.identifier.scopus2-s2.0-85128465189en_US
dc.identifier.wosqualityQ2en_US
dc.identifier.doi10.1016/j.cellsig.2022.110323en_US
dc.identifier.scopusqualityN/Aen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US


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