Mitochondrial energy metabolism and redox state in dyslipidemias (2007)
- Authors:
- Autor USP: KOWALTOWSKI, ALICIA JULIANA - IQ
- Unidade: IQ
- Subjects: MITOCÔNDRIAS; HIPERLIPIDEMIA; RADICAIS LIVRES; ESTRESSE OXIDATIVO
- Language: Inglês
- Imprenta:
- Publisher place: Philadelphia
- Date published: 2007
- Source:
- Título do periódico: IUBMB Life (International Union of Biochemistry and Molecular Biology: Life)
- ISSN: 1521-6543
- Volume/Número/Paginação/Ano: v. 59, n. 4, p. 263-268, 2007
-
ABNT
VERCESI, Anibal Eugenio et al. Mitochondrial energy metabolism and redox state in dyslipidemias. IUBMB Life (International Union of Biochemistry and Molecular Biology: Life), v. 59, n. 4, p. 263-268, 2007Tradução . . Acesso em: 24 abr. 2024. -
APA
Vercesi, A. E., Castilho, R. F., Kowaltowski, A. J., & Oliveira, H. C. F. de. (2007). Mitochondrial energy metabolism and redox state in dyslipidemias. IUBMB Life (International Union of Biochemistry and Molecular Biology: Life), 59( 4), 263-268. -
NLM
Vercesi AE, Castilho RF, Kowaltowski AJ, Oliveira HCF de. Mitochondrial energy metabolism and redox state in dyslipidemias. IUBMB Life (International Union of Biochemistry and Molecular Biology: Life). 2007 ; 59( 4): 263-268.[citado 2024 abr. 24 ] -
Vancouver
Vercesi AE, Castilho RF, Kowaltowski AJ, Oliveira HCF de. Mitochondrial energy metabolism and redox state in dyslipidemias. IUBMB Life (International Union of Biochemistry and Molecular Biology: Life). 2007 ; 59( 4): 263-268.[citado 2024 abr. 24 ] - 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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