Sci. Signal., 2 June 2009
Science, AAAS, Cambridge CB2 1LQ, UK
Several human neurodegenerative diseases, such as Alzheimers and Huntingtons, are caused by aberrant protein aggregation. These disorders typically develop after the fifth decade of life, suggesting a connection with the aging process. In a number of different species, life span can be extended by dietary restriction and reduced insulin and insulin-like growth factor–1 (IGF-1) signaling. These pathways can also decrease toxic protein aggregation, mechanistically linking aging with proteotoxic diseases. While searching for regulators of proteotoxicity in Caenorhabditis elegans, Mehta et al. found that reduction of the von Hippel–Lindau tumor suppressor homolog VHL-1 significantly increased life span and enhanced resistance to proteotoxicity. VHL-1 is an E3 ubiquitin ligase that negatively regulates the hypoxic response, and animals grown under hypoxic conditions lived longer. This alternative longevity pathway was distinct from both dietary restriction and insulin/IGF-1–like signaling.
R. Mehta, K. A. Steinkraus, G. L. Sutphin, F. J. Ramos, L. S. Shamieh, A. Huh, C. Davis, D. Chandler-Brown, M. Kaeberlein, Proteasomal regulation of the hypoxic response modulates aging in C. elegans. Science 324, 1196–1198 (2009). [Abstract] [Full Text]
Citation: H. Pickersgill, Anti-Aging. Sci. Signal. 2, ec186 (2009).
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