About this Research Topic
Mitochondria have been implicated in aging since the 1950s. The dominant view has been that the reactive oxygen species (ROS) generated as a by-product of respiration damage cell molecules and structures and that this damage accumulates to levels that ultimately compromise function. This prevalent view has been questioned recently. Over the past two decades, however, a new paradigm has emerged, in which the role of mitochondria in aging is more nuanced. Intracellular signaling from mitochondria to the nucleus has been shown to play a role in aging from yeast to human. This signaling is triggered by mitochondrial dysfunction that increases with age, and it can compensate for it. On the other hand, mitochondrial deficits are the cause of several human disorders. In the case of age-related macular degeneration, the mitochondrial genotype influences the nuclear gene expression changes that mitochondria signal. In addition to the interaction of mitochondria with the nucleus, there are other interorganelle interactions that involve the mitochondria that impact aging as well as the development of chronic, age-related disorders. These interactions involve lysosomes (vacuoles in yeast) and the endoplasmic reticulum (ER). Thus, the repertoire of interorganelle communication that has an influence on aging is quite diverse. The known examples of such interactions may reflect the proverbial tip of the iceberg.
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