Researchers here report on the identification of a mechanism in mice that amplifies the harms done by an excess of oxidative molecules. Aging is accompanied by a general increase in oxidative stress in cells, and suppressing this amplication mechanism is shown to improve measures of health and slow the progression of aspects of aging. This is similar in spirit to a number of other lines of research that seek to attenuate oxidative stress in old tissue, such as the use of mitochondrially targeted antioxidants, but tackling the challenge at a completely different point of action. Arguably none of this addresses root causes: rising levels of oxidative stress are a consequence of lower level forms of damage and change in aging. So we should expect the scope of benefits to be limited; the results of mitochondrially targeted antioxidants in flies and mice over the past decade might set the expected ballpark.
Aging is characterized by a number of physiological changes including loss of cell division, oxidative stress, DNA damage, nuclear changes, and increased expression of senescence-associated genes. It has been known for some time that oxidant stress plays a central role in
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