Calorie restriction promotes cardiolipin biosynthesis and distribution between mitochondrial membranes (2017)
- Authors:
- USP affiliated authors: WATANABE, II SEI - ICB ; KOWALTOWSKI, ALÍCIA JULIANA - IQ
- Unidades: ICB; IQ
- DOI: 10.1016/j.mad.2017.02.004
- Subjects: MITOCÔNDRIAS; FOSFOLIPÍDEOS
- Language: Inglês
- Imprenta:
- Source:
- Título do periódico: Mechanisms of Ageing and Development
- ISSN: 0047-6374
- Volume/Número/Paginação/Ano: v. 162, p. 9-17, 2017
- Este periódico é de assinatura
- Este artigo NÃO é de acesso aberto
- Cor do Acesso Aberto: closed
-
ABNT
MARTINEZ, Luis Alberto Luevano et al. Calorie restriction promotes cardiolipin biosynthesis and distribution between mitochondrial membranes. Mechanisms of Ageing and Development, v. 162, p. 9-17, 2017Tradução . . Disponível em: https://doi.org/10.1016/j.mad.2017.02.004. Acesso em: 19 abr. 2024. -
APA
Martinez, L. A. L., Forni, M. F., Peloggia, J., Watanabe, I. -S., & Kowaltowski, A. J. (2017). Calorie restriction promotes cardiolipin biosynthesis and distribution between mitochondrial membranes. Mechanisms of Ageing and Development, 162, 9-17. doi:10.1016/j.mad.2017.02.004 -
NLM
Martinez LAL, Forni MF, Peloggia J, Watanabe I-S, Kowaltowski AJ. Calorie restriction promotes cardiolipin biosynthesis and distribution between mitochondrial membranes [Internet]. Mechanisms of Ageing and Development. 2017 ; 162 9-17.[citado 2024 abr. 19 ] Available from: https://doi.org/10.1016/j.mad.2017.02.004 -
Vancouver
Martinez LAL, Forni MF, Peloggia J, Watanabe I-S, Kowaltowski AJ. Calorie restriction promotes cardiolipin biosynthesis and distribution between mitochondrial membranes [Internet]. Mechanisms of Ageing and Development. 2017 ; 162 9-17.[citado 2024 abr. 19 ] Available from: https://doi.org/10.1016/j.mad.2017.02.004 - 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: 10.1016/j.mad.2017.02.004 (Fonte: oaDOI API)
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