Calorie restriction activates the biosynthesis of cardiolipin and its distribution between menbranes (2016)
- Authors:
- Autor USP: KOWALTOWSKI, ALÍCIA JULIANA - IQ
- Unidade: IQ
- Subjects: FOSFOLIPÍDEOS; MITOCÔNDRIAS
- Language: Inglês
- Imprenta:
- Publisher: Sociedade Brasileira de Bioquímica e Biologia Molecular (SBBq)
- Publisher place: Natal
- Date published: 2016
- Source:
- Título do periódico: Abstracts
- Conference titles: Annual Meeting of the Brazilian Society for Biochemistry and Molecular Biology (SBBq)
-
ABNT
MARTINEZ, Luis Alberto Luevano et al. Calorie restriction activates the biosynthesis of cardiolipin and its distribution between menbranes. 2016, Anais.. Natal: Sociedade Brasileira de Bioquímica e Biologia Molecular (SBBq), 2016. . Acesso em: 26 abr. 2024. -
APA
Martinez, L. A. L., Forni, M. F., Peloggia, J., & Kowaltowski, A. J. (2016). Calorie restriction activates the biosynthesis of cardiolipin and its distribution between menbranes. In Abstracts. Natal: Sociedade Brasileira de Bioquímica e Biologia Molecular (SBBq). -
NLM
Martinez LAL, Forni MF, Peloggia J, Kowaltowski AJ. Calorie restriction activates the biosynthesis of cardiolipin and its distribution between menbranes. Abstracts. 2016 ;[citado 2024 abr. 26 ] -
Vancouver
Martinez LAL, Forni MF, Peloggia J, Kowaltowski AJ. Calorie restriction activates the biosynthesis of cardiolipin and its distribution between menbranes. Abstracts. 2016 ;[citado 2024 abr. 26 ] - 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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