Vascular injury in diabetic db/db mice is ameliorated by atorvastatin: role of Rac1/2-sensitive Nox-dependent pathways (2015)
- Authors:
- Autor USP: PASSAGLIA, RITA DE CASSIA ALEIXO TOSTES - FMRP
- Unidade: FMRP
- DOI: 10.1042/CS20140456
- Subjects: DIABETES MELLITUS (FISIOPATOLOGIA); LEPTINA; VASODILATAÇÃO (FARMACOLOGIA); PROTEÍNAS QUINASES; ARTÉRIAS (EFEITOS DE DROGAS)
- Language: Inglês
- Imprenta:
- Source:
- Título do periódico: Clinical Science
- ISSN: 0143-5221
- Volume/Número/Paginação/Ano: v. 128, n. 7, p. 411-423, 2015
- Este periódico é de assinatura
- Este artigo NÃO é de acesso aberto
- Cor do Acesso Aberto: closed
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ABNT
BRUDER-NASCIMENTO, Thiago et al. Vascular injury in diabetic db/db mice is ameliorated by atorvastatin: role of Rac1/2-sensitive Nox-dependent pathways. Clinical Science, v. 128, n. 7, p. 411-423, 2015Tradução . . Disponível em: https://doi.org/10.1042/CS20140456. Acesso em: 18 abr. 2024. -
APA
Bruder-Nascimento, T., Callera, G. E., Montezano, A. C., He, Y., Antunes, T. T., Cat, A. N. D., et al. (2015). Vascular injury in diabetic db/db mice is ameliorated by atorvastatin: role of Rac1/2-sensitive Nox-dependent pathways. Clinical Science, 128( 7), 411-423. doi:10.1042/CS20140456 -
NLM
Bruder-Nascimento T, Callera GE, Montezano AC, He Y, Antunes TT, Cat AND, Tostes R de CA, Touyz RM. Vascular injury in diabetic db/db mice is ameliorated by atorvastatin: role of Rac1/2-sensitive Nox-dependent pathways [Internet]. Clinical Science. 2015 ; 128( 7): 411-423.[citado 2024 abr. 18 ] Available from: https://doi.org/10.1042/CS20140456 -
Vancouver
Bruder-Nascimento T, Callera GE, Montezano AC, He Y, Antunes TT, Cat AND, Tostes R de CA, Touyz RM. Vascular injury in diabetic db/db mice is ameliorated by atorvastatin: role of Rac1/2-sensitive Nox-dependent pathways [Internet]. Clinical Science. 2015 ; 128( 7): 411-423.[citado 2024 abr. 18 ] Available from: https://doi.org/10.1042/CS20140456 - ET-1-induced oxidative stress in doca-salt hypertension involves NAD(P)H oxidase-independent mechanisms
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Informações sobre o DOI: 10.1042/CS20140456 (Fonte: oaDOI API)
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