Pharmacological and physiological stimuli do not promote 'Ca POT. 2+'-sensitive 'K POT. +' channel activity in isolated heart mitochondria (2007)
- Authors:
- Autor USP: KOWALTOWSKI, ALICIA JULIANA - IQ
- Unidade: IQ
- Subjects: MITOCÔNDRIAS; ISQUEMIA; BIOQUÍMICA
- Language: Inglês
- Imprenta:
- Source:
- Título do periódico: Cardiovascular Research
- ISSN: 0008-6363
- Volume/Número/Paginação/Ano: v. 73, n. 4, p. 720-728, 2007
-
ABNT
CANCHERINI, Douglas Vasconcelos e QUELICONI, Bruno Barros e KOWALTOWSKI, Alicia Juliana. Pharmacological and physiological stimuli do not promote 'Ca POT. 2+'-sensitive 'K POT. +' channel activity in isolated heart mitochondria. Cardiovascular Research, v. 73, n. 4, p. 720-728, 2007Tradução . . Acesso em: 16 abr. 2024. -
APA
Cancherini, D. V., Queliconi, B. B., & Kowaltowski, A. J. (2007). Pharmacological and physiological stimuli do not promote 'Ca POT. 2+'-sensitive 'K POT. +' channel activity in isolated heart mitochondria. Cardiovascular Research, 73( 4), 720-728. -
NLM
Cancherini DV, Queliconi BB, Kowaltowski AJ. Pharmacological and physiological stimuli do not promote 'Ca POT. 2+'-sensitive 'K POT. +' channel activity in isolated heart mitochondria. Cardiovascular Research. 2007 ; 73( 4): 720-728.[citado 2024 abr. 16 ] -
Vancouver
Cancherini DV, Queliconi BB, Kowaltowski AJ. Pharmacological and physiological stimuli do not promote 'Ca POT. 2+'-sensitive 'K POT. +' channel activity in isolated heart mitochondria. Cardiovascular Research. 2007 ; 73( 4): 720-728.[citado 2024 abr. 16 ] - 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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