Nrf2/ARE Pathway Modulation by Dietary Energy Regulation in Neurological Disorders

Autor(es)

Vasconcelos, Andrea Rodrigues ^[1] ; dos Santos, Nilton Barreto ^[2] ; Scavone, Cristoforo ^[1] ; Munhoz, Carolina Demarchi ^[2]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Inst Biomed Sci, Dept Pharmacol, Lab Mol Neuropharmacol, Sao Paulo - Brazil

^[2] Univ Sao Paulo, Inst Biomed Sci, Dept Pharmacol, Lab Neuroendocrinopharmacol & Immunomodulat, Sao Paulo - Brazil

• Tipo de documento: Artigo de Revisão
• Fonte: FRONTIERS IN PHARMACOLOGY; v. 10, FEB 4 2019.
• Citações Web of Science: 4

Resumo

Nuclear factor erythroid 2-related factor 2 (Nrf2) regulates the expression of an array of enzymes with important detoxifying and antioxidant functions. Current findings support the role of high levels of oxidative stress in the pathogenesis of neurological disorders. Given the central role played by Nrf2 in counteracting oxidative damage, a number of studies have targeted the modulation of this transcription factor in order to confer neuroprotection. Nrf2 activity is tightly regulated by oxidative stress and energy-based stimuli. Thus, many dietary interventions based on energy intake regulation, such as dietary energy restriction (DER) or high-fat diet (HFD), modulate Nrf2 with consequences for a variety of cellular processes that affect brain health. DER, by either restricting calorie intake or meal frequency, activates Nrf2 thereby triggering its protective effects, whilst HFD inhibit this pathway, thereby exacerbating oxidative stress. Consequently, DER protocols can be valuable strategies in the management of central nervous system (CNS) disorders. Herein, we review current knowledge of the role of Nrf2 signaling in neurological diseases, namely Alzheimer's disease, Parkinson's disease, multiple sclerosis and cerebral ischemia, as well as the potential of energy (i)ntake regulation in the management of Nrf2 signaling. (AU)

• Processo FAPESP: 16/07427-8 - Envelhecimento e neuroproteção: ações da proteína Klotho no metabolismo energético, sinalização da Na,K-ATPase e respostas adaptativas no sistema nervoso central
• Beneficiário: Cristoforo Scavone
• Modalidade de apoio: Auxílio à Pesquisa - Temático
• Processo FAPESP: 12/24727-4 - Avaliação dos efeitos terapêuticos da dexametasona (análogo sintético de glicocorticóides) e G1 (agonista do receptor de estrógeno acoplado a proteína G, GPER-1) na neuro-inflamação desencadeada por encefalomielite autoimune experimental
• Beneficiário: Carolina Demarchi Munhoz
• Modalidade de apoio: Auxílio à Pesquisa - Regular