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Premature aging in klotho mutant mice: cause or consequence?

Beate Lanske¹, M Shawkat Razzaque

¹Department of Developmental Biology, Harvard School of Dental Medicine, Research and Educational Building, 190 Longwood Avenue, Boston, MA 02115, USA. beate_lanske@hsdm.harvard.edu

Ageing Research Reviews

|March 14, 2007

Summary

Fibroblast growth factor 23 (Fgf-23) and klotho are key regulators of aging. Klotho acts as a cofactor for Fgf-23, explaining why klotho-deficient mice exhibit premature aging phenotypes.

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Area of Science:

Gerontology and Molecular Biology
Genetics and Developmental Biology

Background:

Mammalian models are crucial for studying aging mechanisms.
Fibroblast growth factor 23 (Fgf-23) null mice and klotho hypomorphs exhibit premature aging phenotypes.

Purpose of the Study:

To investigate the molecular mechanisms underlying premature aging in mouse models.
To elucidate the relationship between Fgf-23 and klotho in aging processes.

Main Methods:

Comparative analysis of Fgf-23 null mice and klotho hypomorphs.
Examination of in vivo phenotypes, including lifespan, fertility, and tissue pathology.
Biochemical and morphological assessments of aging markers.

Main Results:

Both Fgf-23 null mice and klotho hypomorphs display similar premature aging features.
Klotho acts as a necessary cofactor for Fgf-23 signaling.
Klotho deficiency impairs Fgf-23 bioactivity, leading to aging phenotypes.

Conclusions:

Premature aging in klotho-deficient mice is a consequence of impaired Fgf-23 activity.
Fgf-23 and klotho signaling pathways are interconnected in regulating aging.
Klotho's role as an aging factor is redefined through its function as an Fgf-23 cofactor.