Nrf2–ARE pathway: An emerging target against oxidative stress and neuroinflammation in neurodegenerative diseases

dc.contributor.authorBuendia, Izaskun
dc.contributor.authorMichalska Dziama, Patrycja
dc.contributor.authorNavarro González De Mesa, Elisa
dc.contributor.authorGameiro, Isabel
dc.contributor.authorEgea, Javier
dc.contributor.authorLeón Martínez, Rafael
dc.date.accessioned2024-01-29T09:03:44Z
dc.date.available2024-01-29T09:03:44Z
dc.date.issued2016-01-01
dc.description.abstractNeurodegenerative diseases (NDDs) are predicted to be the biggest health concern in this century and the second leading cause of death by 2050. The main risk factor of these diseases is aging, and as the aging population in Western societies is increasing, the prevalence of these diseases is augmenting exponentially. Despite the great efforts to find a cure, current treatments remain ineffective or have low efficacy. Increasing lines of evidence point to exacerbated oxidative stress, mitochondrial dysfunction and chronic neuroinflammation as common pathological mechanisms underlying neurodegeneration. We will address the role of the nuclear factor E2-related factor 2 (Nrf2) as a potential target for the treatment of NDDs. The Nrf2–ARE pathway is an intrinsic mechanism of defence against oxidative stress. Nrf2 is a transcription factor that induces the expression of a great number of cytoprotective and detoxificant genes. There are many evidences that highlight the protective role of the Nrf2–ARE pathway in neurodegenerative conditions, as it reduces oxidative stress and neuroinflammation. Therefore, the Nrf2 pathway is being increasingly considered a therapeutic target for NDDs. Herein we will review the deregulation of the Nrf2 pathway in different NDDs and the recent studies with Nrf2 inducers as “proof-of-concept” for the treatment of those devastating pathologies.
dc.description.departmentDepto. de Química en Ciencias Farmacéuticas
dc.description.facultyFac. de Farmacia
dc.description.refereedTRUE
dc.description.sponsorshipFundación Teófilo Hernando
dc.description.sponsorshipEuropean Commission
dc.description.sponsorshipInstituto de Salud Carlos III
dc.description.statuspub
dc.identifier.citationBuendia I, Michalska P, Navarro E, Gameiro I, Egea J, León R. Nrf2–ARE pathway: An emerging target against oxidative stress and neuroinflammation in neurodegenerative diseases. Pharmacology & Therapeutics 2016;157:84–104. https://doi.org/10.1016/j.pharmthera.2015.11.003.
dc.identifier.doi10.1016/j.pharmthera.2015.11.003
dc.identifier.issn0163-7258
dc.identifier.officialurlhttps://doi.org/10.1016/j.pharmthera.2015.11.003
dc.identifier.urihttps://hdl.handle.net/20.500.14352/95760
dc.journal.titlePharmacology & Therapeutics
dc.language.isoeng
dc.page.final104
dc.page.initial84
dc.relation.projectIDinfo:eu-repo/grantAgreement/PCIG11-GA-2012-322156
dc.relation.projectIDinfo:eu-repo/grantAgreement/MINECO//PI14%2F00372/ES/Compuestos muldidiana quirales para el tratamiento de enfermedades neurodegenerativas: ligandos de receptores nicotínicos, inductores de Nrf2 y anti-inflamatorios/
dc.relation.projectIDinfo:eu-repo/grantAgreement/MICINN//CP11%2F00165/ES/CP11%2F00165/
dc.relation.projectIDinfo:eu-repo/grantAgreement/MINECO//CP14%2F00008/ES/CP14%2F00008/
dc.relation.projectIDinfo:eu-repo/grantAgreement/AP2010-1219
dc.relation.projectIDinfo:eu-repo/grantAgreement/MECD//FPU13%2F03737/ES/FPU13%2F03737/
dc.rights.accessRightsrestricted access
dc.subject.cdu615:54
dc.subject.cdu615.31
dc.subject.keywordNeurodegenerative diseases
dc.subject.keywordOxidative stress
dc.subject.keywordNeuroinflammation
dc.subject.keywordNuclear factor E2-related factor 2Nrf2
dc.subject.keywordElectrophile response elements
dc.subject.keywordPhase II antioxidant response
dc.subject.keywordNrf2-inducers
dc.subject.ucmQuímica farmaceútica
dc.subject.unesco3209.99 Otras
dc.titleNrf2–ARE pathway: An emerging target against oxidative stress and neuroinflammation in neurodegenerative diseases
dc.typejournal article
dc.type.hasVersionVoR
dc.volume.number157
dspace.entity.typePublication
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relation.isAuthorOfPublicationd0e22d4d-2011-4a9f-bd9c-609855dba391
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relation.isAuthorOfPublication.latestForDiscovery7093c6ce-e368-44f0-a993-8f7212cb1c2a
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