Mild mitochondrial uncoupling and calorie restriction increase fasting eNOS, Akt and mitochondrial biogenesis (2011)
- Authors:
- Autor USP: KOWALTOWSKI, ALICIA JULIANA - IQ
- Unidade: IQ
- DOI: 10.1371/journal.pone.0018433
- Subjects: ÓXIDO NÍTRICO; EXPRESSÃO GÊNICA; MITOCÔNDRIAS
- Language: Inglês
- Imprenta:
- Publisher place: San Francisco
- Date published: 2011
- Source:
- Este periódico é de acesso aberto
- Este artigo é de acesso aberto
- URL de acesso aberto
- Cor do Acesso Aberto: gold
- Licença: cc-by
-
ABNT
CERQUEIRA, Fernanda Menezes e LAURINDO, Francisco Rafael Martins e KOWALTOWSKI, Alicia Juliana. Mild mitochondrial uncoupling and calorie restriction increase fasting eNOS, Akt and mitochondrial biogenesis. PLOS ONE, v. 6, n. 3, p. 1-5 art. e18433, 2011Tradução . . Disponível em: https://doi.org/10.1371/journal.pone.0018433. Acesso em: 20 abr. 2024. -
APA
Cerqueira, F. M., Laurindo, F. R. M., & Kowaltowski, A. J. (2011). Mild mitochondrial uncoupling and calorie restriction increase fasting eNOS, Akt and mitochondrial biogenesis. PLOS ONE, 6( 3), 1-5 art. e18433. doi:10.1371/journal.pone.0018433 -
NLM
Cerqueira FM, Laurindo FRM, Kowaltowski AJ. Mild mitochondrial uncoupling and calorie restriction increase fasting eNOS, Akt and mitochondrial biogenesis [Internet]. PLOS ONE. 2011 ; 6( 3): 1-5 art. e18433.[citado 2024 abr. 20 ] Available from: https://doi.org/10.1371/journal.pone.0018433 -
Vancouver
Cerqueira FM, Laurindo FRM, Kowaltowski AJ. Mild mitochondrial uncoupling and calorie restriction increase fasting eNOS, Akt and mitochondrial biogenesis [Internet]. PLOS ONE. 2011 ; 6( 3): 1-5 art. e18433.[citado 2024 abr. 20 ] Available from: https://doi.org/10.1371/journal.pone.0018433 - 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
Informações sobre o DOI: 10.1371/journal.pone.0018433 (Fonte: oaDOI API)
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