The present dominant approach to the development of therapies to treat aging is not, sadly, the SENS rejuvenation research agenda, but instead efforts to persistently activate evolved responses to cellular stress. These mechanisms normally start up in response to exercise, calorie restriction, raised temperature, and the topic here, hypoxia, among other sources of stress. The responses generally lead to some period of more aggressive cellular maintenance, particularly autophagy, responsible for identifying and recycling damaged molecules and structures within the cell.
There is comprehensive evidence to support the idea that running these mechanisms at a higher level all the time, in the absence of stress, is beneficial. It is an aspect of numerous approaches shown to modestly slow aging in various short-lived species over the past few decades. As the authors of this short commentary note, in the case of hypoxia the situation is more complex, however. A number of age-related conditions involve disarray or excessive activation of mechanisms of the hypoxia response. That must be in some way reconciled with the evidence for overactivation of the hypoxia responses to modestly slow aging life in various animal studies.
Regardless, it is the case that enhancement of stress responses doesn’t
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