Reviewing Work on CISD2, a Mammalian Longevity Gene

Few genes have been shown to robustly alter mammalian longevity as a result of altered expression, with data obtained primarily in mice. Klotho is perhaps the most well known and well studied of that small but steadily growing portfolio. The topic of today's open access paper is another of these longevity genes, CISD2. Loss of CISD2 shortens lifespan, while increased expression extends life span in mice. CISD2 is upregulated after exercise, and may act through autophagy, a common factor in many approaches shown to modestly slow aging in laboratory species. Like other approaches to upregulation of autophagy, increased CISD2 expression improves liver function in mice. Recently researchers have extended mouse life span by a small degree via pharmacological approaches to upregulation of CISD2. The authors of the this paper overstate, I think, the level of interest we should have in CISD2 upregulation as a basis for therapy. Any form of upregulation of autophagy might be described as a calorie restriction mimetic strategy, given that increased autophagy appears to be the primary means by which calorie restriction produces benefits to health and longevity. While calorie restriction improves health in humans, it certainly does not move the needle on life span in long-lived mammals the same way it does in short-lived mammals. The underlying reasons for this difference have yet to be established in any detail, but this is why we should be skeptical of most of the methods of slo...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs