Klotho, Aging, and the Failing Kidney.
Level 5 - mechanism / opinion, no new human data
Narrative review of biological mechanisms and potential therapeutic strategies without systematic search or original human data.
PubMed 32982966 · doi:10.3389/fendo.2020.00560
What was done
This narrative review summarizes the role of the α-Klotho protein and Fibroblast Growth Factor-23 (FGF23) signaling in phosphate homeostasis, vitamin D metabolism, mammalian aging, and chronic kidney disease. It outlines potential senotherapeutic strategies to restore or enhance Klotho expression, including exogenous administration, agonists, dietary changes, and gut microbiome modulation.
What was found
The abstract provides no quantitative data or numerical outcomes. It reports that α-Klotho serves as the receptor for FGF23, that Klotho levels decline with advancing age alongside increasing phosphate toxicity, and that Klotho deficiency is directly involved in chronic kidney disease pathophysiology.
Why it matters
It conceptualizes Klotho as a central mechanistic target connecting mineral metabolism, renal failure, and systemic aging, framing several emerging senotherapeutic approaches for intervention.
Limits
The abstract provides no empirical data, sample sizes, or quantitative metrics. As a narrative review, it lacks a systematic search protocol and does not present direct clinical trial evidence in humans.
Cited by
- supports Alpha-Klotho acts on cellular aging through phosphate and vitamin D metabolism pathways.