Ageing is a fundamental, unsolved mystery in biology. DAF-16, a FOXO-family transcription factor, influences the rate of ageing of Caenorhabditis elegans [The transcription factor HSF-1, which regulates the heat-shock response, also influences aging. Murphy, Coleen T., et al. "Genes that act downstream of DAF-16 to influence the lifespan of Caenorhabditis elegans." Nature 424.6946 (2003): 277-283.]. Dr. Hsu and co-authors have shown that reducing HSF-1 activity accelerates tissue aging and shortens life-span, and HSF-1 overexpression extends lifespan. It is suggested that this is because HSF-1 and DAF-16 together activate expression of specific genes, including genes encoding small heat-shock proteins, which in turn promote longevity. The small heat-shock proteins also delay the onset of polyglutamine-expansion protein aggregation, suggesting that these proteins couple the normal aging process to this type of age-related disease [Hsu, Ao-Lin, Coleen T. Murphy, and Cynthia Kenyon. "Regulation of aging and age-related disease by DAF-16 and heat-shock factor." Science 300.5622 (2003): 1142-1145.]. Daf-16 gene encodes multiple isoforms that are expressed in distinct tissue types and are probable orthologs of human FKHRL1, FKHR, and AFX [Lee, Raymond YN, Jürgen Hench, and Gary Ruvkun. "Regulation of C. elegans DAF-16 and its human ortholog FKHRL1 by the daf-2 insulin-like signaling pathway." Current Biology 11.24 (2001): 1950-1957.]. Gene HSF-1 is known in human. All in all, drugs that upregulate genes DAF-16 (or its homologs) and HSF-1 could make the life much longer.
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