Removing an enzyme eased kidney aging and bone loss in mice
Deleting the enzyme’s gene in kidney filtering cells reduced kidney damage and age-related bone loss in aged mice; a drug also improved kidney and bone measures.
Limit: The drug experiment lasted two months, too short to assess long-term safety
Edited by Boris Djordjevic · AgingResearch.News
In experiments in aged mice, researchers deleted Ptges2, the gene for the enzyme microsomal prostaglandin E synthase-2, throughout the body or in specific kidney cells. Whole-body deletion prolonged median survival and reduced kidney scarring and injury.
Deleting the gene in podocytes, cells that help filter blood, reduced kidney injury and senescence, a state in which cells stop dividing. Deletion in kidney tubule cells had smaller benefits. Podocyte-specific deletion also reduced age-related osteoporosis, a disease that weakens bones. The authors proposed that impaired kidney hormone function helped connect kidney aging to bone loss. In a separate experiment, 20-month-old mice received the enzyme-blocking drug SZ0232 or saline for two months. Researchers injected 0.5 milligrams per kilogram every two days. The drug reduced kidney aging measures and improved bone structure. The researchers reported no overt adverse effects on major organs with either approach.
Why it matters
Kidney aging can disrupt functions beyond blood filtration. This work bears on whether targeting processes in the kidney could help address age-related osteoporosis.
Caveats
The intervention evidence came from mice, not people. The two-month drug experiment cannot establish long-term safety.
The paper
Podocyte mPGES-2 Determines Renal Aging and Contributes to Senile Osteoporosis
Xuzhou Medical College
Aging Cell, Jun 25, 2026, Open access
