Time-dependent impairments of mitochondrial function play a key role in biological aging. Work on fungal aging models has been instrumental in unraveling basic mechanisms leading to mitochondrial dysfunction and the identification of different pathways active in keeping mitochondria 'healthy' over time. Pathways including those involved in reactive oxygen scavenging, repair of damage, proteostasis, mitochondrial dynamics, and biogenesis, are interconnected and part of a complex quality control system. The individual components of this network are limited in capacity. However, if the capacity of one pathway is overwhelmed, another one may be activated. The mechanisms controlling the underlying cross-talk are poorly understood and subject of intensive investigation.
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