Nox1 in cardiovascular diseases: regulation and pathophysiology

Autor(es)

Gimenez, Marcela ^{[1, 2]} ; Schickling, Brandon M. ^[2] ; Lopes, Lucia R. ^[1] ; Miller, Jr., Francis J. ^{[2, 3]}

Afiliação do(s) autor(es)

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

^[2] Univ Iowa, Dept Internal Med, Iowa City, IA 52242 - USA

^[3] Vet Affairs Med Ctr Iowa City, Iowa City, IA 52246 - USA

• Tipo de documento: Artigo de Revisão
• Fonte: Clinical Science; v. 130, n. 3, p. 151-165, FEB 1 2016.
• Citações Web of Science: 16

Resumo

Since its discovery in 1999, a number of studies have evaluated the role of Nox1 NADPH oxidase in the cardiovascular system. Nox1 is activated in vascular cells in response to several different agonists, with its activity regulated at the transcriptional level as well as by NADPH oxidase complex formation, protein stabilization and post-translational modification. Nox1 has been shown to decrease the bioavailability of nitric oxide, transactivate the epidermal growth factor receptor, induce pro-inflammatory signalling, and promote cell migration and proliferation. Enhanced expression and activity of Nox1 under pathologic conditions results in excessive production of reactive oxygen species and dysregulated cellular function. Indeed, studies using genetic models of Nox1 deficiency or overexpression have revealed roles for Nox1 in the pathogenesis of cardiovascular diseases ranging from atherosclerosis to hypertension, restenosis and ischaemia/reperfusion injury. These data suggest that Nox1 is a potential therapeutic target for vascular disease, and drug development efforts are ongoing to identify a specific bioavailable inhibitor of Nox1. (AU)

• Processo FAPESP: 13/18300-0 - Papel da Dissulfeto Isomerase Proteíca na regulação redox da ativação de ADAM17 e sinalização de EGFR em doença vascular
• Beneficiário: Marcela Gimenez
• Modalidade de apoio: Bolsas no Exterior - Estágio de Pesquisa - Pós-Doutorado
• Processo FAPESP: 13/03520-5 - Papel da proteína dissulfeto isomerase na geração de espécies reativas de oxigênio pela NADPH oxidase durante o desenvolvimento da hipertensão arterial
• Beneficiário: Lucia Rossetti Lopes
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 13/07937-8 - Redoxoma
• Beneficiário: Ohara Augusto
• Modalidade de apoio: Auxílio à Pesquisa - Centros de Pesquisa, Inovação e Difusão - CEPIDs
• Processo FAPESP: 09/54764-6 - Regulação da homeostase redox e resposta integrada a estresse pela dissulfeto isomerase protéica (PDI): mecanismos e papel na fisiopatologia e terapêutica de doenças vasculares
• Beneficiário: Francisco Rafael Martins Laurindo
• Modalidade de apoio: Auxílio à Pesquisa - Temático