How mitochondrial complex II inhibition promotes neuronal damage (2004)
- Autores:
- Maciel, Evelise Neves - Universidade Estadual de Campinas (UNICAMP)
- Kowaltowski, Alicia Juliana
- Schwalm, Fábio Duarte - Universidade Federal do Rio Grande do Sul (UFRGS)
- Rodrigues, Juliana M. - Universidade Federal do Rio Grande do Sul (UFRGS)
- Souza, Diogo Onofre - Universidade Federal do Rio Grande do Sul (UFRGS)
- Vercesi, Anibal Eugenio - Universidade Estadual de Campinas (UNICAMP)
- Wajner, Moacir - Universidade Federal do Rio Grande do Sul (UFRGS)
- Castilho, Roger Frigério - Universidade Estadual de Campinas (UNICAMP)
- Autor USP: KOWALTOWSKI, ALICIA JULIANA - IQ
- Unidade: IQ
- Assuntos: BIOQUÍMICA; MITOCÔNDRIAS
- Idioma: Inglês
- Imprenta:
- Fonte:
- Título do periódico: Abstracts
- Nome do evento: Congress of the Brazilian Society for Cell Biology
-
ABNT
MACIEL, Evelise Neves et al. How mitochondrial complex II inhibition promotes neuronal damage. 2004, Anais.. São Paulo: SBBC, 2004. . Acesso em: 27 abr. 2024. -
APA
Maciel, E. N., Kowaltowski, A. J., Schwalm, F. D., Rodrigues, J. M., Souza, D. O., Vercesi, A. E., et al. (2004). How mitochondrial complex II inhibition promotes neuronal damage. In Abstracts. São Paulo: SBBC. -
NLM
Maciel EN, Kowaltowski AJ, Schwalm FD, Rodrigues JM, Souza DO, Vercesi AE, Wajner M, Castilho RF. How mitochondrial complex II inhibition promotes neuronal damage. Abstracts. 2004 ;[citado 2024 abr. 27 ] -
Vancouver
Maciel EN, Kowaltowski AJ, Schwalm FD, Rodrigues JM, Souza DO, Vercesi AE, Wajner M, Castilho RF. How mitochondrial complex II inhibition promotes neuronal damage. Abstracts. 2004 ;[citado 2024 abr. 27 ] - Caloric restriction protects mice against isoproterenol-induced cardiac hypertrophy by mechanisms that involve mitochondrial ATP sensitive potassium channel and modulation of redox state
- Bioenergetic consequences of opening the ATP-sensitive `K POT. +´ channel of heart mitochondria
- Mechanisms by which opening the mitochondrial ATP- sensitive 'K POT. +' channel protects the ischemic heart
- Effect of Bcl-2 overexpression on mitochondrial structure and function
- Mitochondrial ATP-sensitive 'K POT. +' channel opening decreases reactive oxygen species generation
- Mitochondrial channels that regulate cell viability
- Mitochondrial permeability transition is delayed by ATP-sensitive 'K POT. +' channel ('Mitok IND. ATP') opening
- Protection against ischemic brain injury by inhibition of mitochondrial oxidative stress
- ATP-sensitive K+ channel (mitoKATP) opening protects against cellular damage preventing mitochondrial permeability transition
- Diet, mitochondria and energy metabolism
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