Two interventions eased age-related kidney damage in mice
Experiments in 92-week-old male mice suggested a link between molecules that accumulate with age and a protein elevated in chronic kidney disease.
Limit: The abstract omits mouse group sizes, doses, and intervention duration
Edited by Boris Djordjevic · AgingResearch.News
Naturally aged male C57BL/6 mice, 92 weeks old, received either aminoguanidine or an antibody in experiments on kidney aging. Aminoguanidine inhibits the formation of advanced glycation end products, molecules that accumulate over time. The antibody neutralizes insulin-like growth factor binding protein-3, or IGFBP-3, a protein elevated in chronic kidney disease.
Both interventions reduced age-associated kidney dysfunction, structural deterioration and the buildup of collagen, a structural protein. Each also reduced the buildup of advanced glycation end products and levels of IGFBP-3, suggesting that the two processes interact. The researchers also examined an array of human kidney tissue samples spanning a broad age range. Kidneys from elderly donors had markedly higher levels of IGFBP-3 and one major advanced glycation end product.
Why it matters
Chronic kidney disease becomes more common with age. The authors proposed that targeting these linked processes may help limit its progression in older people.
Caveats
The intervention results came from male mice, not people; the human tissue analysis was observational. The abstract does not report mouse group sizes, doses or intervention duration.
The paper
National Taiwan University
Tissue & Cell, May 15, 2026
