GSK3β and the aging kidney

• Published in: The Journal of clinical investigation Vol. 132; no. 4; pp. 1 - 3
• Main Authors: Kreidberg, Jordan A, Schumacher, Valerie A
• Format: Journal Article
• Language: English
• Published: United States American Society for Clinical Investigation 15.02.2022
• Subjects: Age; Aging; Animal models; Animals; Biomedical research; Cell cycle; Enzymes; Genotype & phenotype; Glucose; Glycogen; Glycogen synthase kinase 3; Glycogen Synthase Kinase 3 - metabolism; Glycogen Synthase Kinase 3 beta - genetics; Glycogen Synthase Kinase 3 beta - metabolism; Kidney; Kidney diseases; Kidney Glomerulus - metabolism; Kinases; Lithium; Metabolism; Mice; Phosphorylation; Population; Senescence
• ISSN: 1558-8238; 0021-9738; 1558-8238
• DOI: 10.1172/JCI155885

Kidney function decreases with age and may soon limit millions of lives as the proportion of the population over 70 years of age increases. Glycogen synthase kinase 3β (GSK3β) is involved with metabolism and may have a role in kidney senescence, positioning it as a target for complications from chronic kidney disease. However, different studies suggest GSK3 has contrasting effects. In this issue of the JCI, Fang et al. explored the function of GSK3β and the interplay with lithium using human tissue and mouse models. Notably, GSK3β was overexpressed and activated in aging mice, and depleting GSK3β reduced senescence and glomerular aging. In this Commentary, we explore the similarities and differences between Fang et al. and previous findings by Hurcombe et al. These findings should prompt further study of lithium and other GSK3β inhibitors as a means of extending glomerular function in individuals with chronic kidney disease.