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SUMOylation In Cerebral Ischaemia

2026-05Recensão Acesso aberto
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dc.contributor.authorGissoni, João M.
dc.contributor.authorCampos, Kiara F.
dc.contributor.authorVieira, Helena L.A.
dc.contributor.authorNetto, Carlos Alexandre
dc.contributor.authorDurán-Carabali, Luz Elena
dc.contributor.authorCimarosti, Helena I.
dc.contributor.institutionUCIBIO - Applied Molecular Biosciences Unit
dc.contributor.institutionDQ - Departamento de Química
dc.contributor.institutionFaculdade de Ciências e Tecnologia (FCT)
dc.contributor.pblWiley
dc.date.accessioned2026-07-16T16:01:04Z
dc.date.available2026-07-16T16:01:04Z
dc.date.issued2026-05
dc.descriptionPublisher Copyright: © 2026 The Author(s). Journal of Neurochemistry published by John Wiley & Sons Ltd on behalf of International Society for Neurochemistry.
dc.description.abstractHypoxia-ischaemia and reperfusion (HI/R) damage is a result stemming from any event that interrupts the brain's blood supply, such as the occlusion of a blood vessel. In neurons, the molecular mechanisms involved in the HI/R cascade are diverse in nature, ranging from proteomic, genomic, and transcriptomic alterations in the cells. Many of these changes are governed by post-translational modifications such as SUMOylation, which can quickly and reversibly alter the fate of key proteins. This review summarises current evidence regarding the role of SUMOylation in key molecular pathways in major in vivo and in vitro models of cerebral HI/R. Our review reinforces the concept of SUMOylation being a dynamic and time-dependent process that functions as a rapid molecular switch, affecting major pathways across different cell types and cellular compartments. Moreover, the context-dependent pathological and neuroprotective action of SUMOylation in different pathways involved in HI/R is explored. It sheds light on a novel notion placing aberrant SUMO-1 conjugation as the main culprit in reperfusion damage, whereas SUMO-2/3 principally serves as a compensatory mechanism during ischaemia to prevent damage. Nevertheless, it also highlights important gaps in the current scientific evidence regarding the role of SUMO, underscoring the need for further investigation. (Figure presented.).en
dc.description.versionpublishersversion
dc.description.versionpublished
dc.format.extent1841119
dc.identifier.doi10.1111/jnc.70472
dc.identifier.issn0022-3042
dc.identifier.otherPURE: 168488599
dc.identifier.otherPURE UUID: 8887115f-aebe-4fd8-a9fc-af0f562dab88
dc.identifier.otherScopus: 105039667412
dc.identifier.otherPubMed: 42175537
dc.identifier.otherWOS: 001777352700020
dc.identifier.urihttp://hdl.handle.net/10362/204603
dc.identifier.urlhttps://www.scopus.com/pages/publications/105039667412
dc.language.isoeng
dc.peerreviewedyes
dc.subjectMCAo
dc.subjectmicroglia
dc.subjectmitochondria
dc.subjectneuroinflammation
dc.subjectneurons
dc.subjectOGD
dc.subjectSUMO
dc.subjectBiochemistry
dc.subjectCellular and Molecular Neuroscience
dc.titleSUMOylation In Cerebral Ischaemiaen
dc.title.subtitleA Dynamic, Isoform-Specific Regulator of Neuroprotection and Injuryen
dc.typereview
degois.publication.issue5
degois.publication.titleJournal of Neurochemistry
degois.publication.volume170
dspace.entity.typePublication
rcaap.rightsopenAccess

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