Mice missing the KDM6A gene in their kidneys show signs of faster aging, like higher levels of certain proteins linked to aging.
Scientific Claim
Downregulation of Klotho and upregulation of aging markers (p53, p21, p16) in kidneys of mice with kidney-specific KDM6A deletion is associated with kidney aging.
Original Statement
“The expression of Klotho was downregulated while expression of aging markers including p53, p21, and p16 was upregulated in kidneys of KDM6A-cKO mice, indicating that deletion of KDM6A in the renal tubule cells promotes kidney aging.”
Evidence Quality Assessment
Claim Status
overstated
Study Design Support
Design cannot support claim
Appropriate Language Strength
association
Can only show association/correlation
Assessment Explanation
Based on abstract only - full methodology not available to verify. The abstract uses causal language ('promotes'), but the study is an animal model without explicit RCT design, so causation cannot be established.
Evidence from Studies
Supporting (1)
KDM6A Demethylase Regulates Renal Sodium Excretion and Blood Pressure