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Mitochondrial form, function and signalling in aging

期刊

BIOCHEMICAL JOURNAL
卷 473, 期 -, 页码 3421-3449

出版社

PORTLAND PRESS LTD
DOI: 10.1042/BCJ20160451

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资金

  1. Fundacao de Amparo a Pesquisa no Estado de Sao Paulo (FAPESP) [2010/51906-1, 2013/51288-1, 2015/15526-3, 2014/17270-3, 2015/25776-7, 2013/ 04871-6, 2013/04919-9]
  2. Centro de Pesquisa
  3. Conselho Nacional de Pesquisa e Desenvolvimento Inovacao e Difusao em Processos Redox em Biomedicina (CEPID Redoxoma) [2013/07937-8]
  4. Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
  5. Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
  6. Nucleo de Apoio a Pesquisa em Processos Redox em Biomedicina (NAP-Redoxoma)
  7. Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [15/25776-7] Funding Source: FAPESP

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Aging is often accompanied by a decline in mitochondrial mass and function in different tissues. Additionally, cell resistance to stress is frequently found to be prevented by higher mitochondrial respiratory capacity. These correlations strongly suggest mitochondria are key players in aging and senescence, acting by regulating energy homeostasis, redox balance and signalling pathways central in these processes. However, mitochondria display a wide array of functions and signalling properties, and the roles of these different characteristics are still widely unexplored. Furthermore, differences in mitochondrial properties and responses between tissues and cell types, and how these affect whole body metabolism are also still poorly understood. This review uncovers aspects of mitochondrial biology that have an impact upon aging in model organisms and selected mammalian cells and tissues.

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