Ccna2 as a Novel Regulator of Cellular Senescence
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Given the present wave of investment into the treatment of aging, in both the business and research communities, and given the significant valuations put on the first companies working on senolytic drugs to clear senescent cells, it should come as no surprise to see a land rush underway in the investigation of the biochemistry of cellular senescence. The state of funding for any specific field of research is to a sizable degree steered by what is going on in the world of startups and venture capital. When finding a new mechanism is a potential ticket to valuable intellectual property, a startup company, and production of clinical therapies, then there will be more funding available for researchers involved in the search for mechanisms, and more researchers joining in.

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Senescent cells are clearly significant in all aspects of aging, and removing them is proving, in mice at least, to produce robust reversal of aging and age-related disease. Senescent cells, while small in number even in old individuals, produce a potent mix of signals known as the senescence-associated secretory phenotype, or SASP. This SASP generates chronic inflammation, changes the behavior of normal cells for the worse, destructively remodels the

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