Biology of Aging: Hormonal Suppression of Aging in Mice
A defect in Klotho gene expression in mice accelerates the
degeneration of multiple age-sensitive traits. New work
demonstrates that overexpression of Klotho in mice extends life
span. Klotho protein functions as a circulating hormone that
binds to a cell-surface receptor and represses intracellular
signals of insulin and insulin-like growth factor-1, an
evolutionarily conserved mechanism for extending life span.
Alleviation of aging-like phenotypes in Klotho-deficient mice was
observed by perturbing insulin and IGF1 signaling, suggesting
that Klotho-mediated inhibition of insulin and IGF1 signaling
contributes to its anti-aging properties. Klotho protein may
function as an anti-aging hormone in mammals.
Full report at http://scienceweek.com/2005/sw051111-5.htm
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Iron chelation and a free radical scavenger suppress angiotensin
II-induced downregulation of klotho, an anti-aging gene, in rat.
Saito K, Ishizaka N, Mitani H, Ohno M, Nagai R
FEBS Lett. 2003 Sep 11; 551(1-3): 58-62
Administration of angiotensin II to rats decreases renal expression of
klotho, an aging-related gene, and also causes abnormal iron deposition
in renal cells. Here we have examined the effects of iron overload and
iron chelation on renal expression of klotho in untreated rats and rats
treated with angiotensin II. Administration of iron-dextran caused a
downregulation of klotho expression, and iron chelation suppressed the
angiotensin II-induced downregulation of this gene. In addition, a free
radical scavenger (T-0970), which effectively decreased plasma levels
of 8-epi-prostaglandin F(2alpha) (8-epi-PGF(2alpha)), suppressed
angiotensin II-induced downregulation of klotho. Collectively, these
findings suggest that abnormal iron metabolism and increased oxidative
stress are involved in the mechanism of angiotensin II-mediated
modulation of klotho expression.
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