Researchers Identify IL-23R as an Aging and Inflammation Biomarker
Scientists at Mayo Clinic have identified a new aging biomarker, the plasma protein IL-23R, which increases with age and decreases in response to drugs targeting senescent cells. Their findings, published in Nature Aging, connect IL-23R to the cellular aging process known as senescence and its role in systemic inflammation.
“Our research is the first to show that IL-23R is an aging biomarker linked to senescence,” says senior author Marissa Schafer, Ph.D. “This discovery could open new pathways for understanding age-related diseases and developing therapeutic strategies.”
IL-23R, a protein known to activate immune cells and trigger inflammation, becomes problematic when overactive, contributing to persistent inflammation seen in conditions like rheumatoid arthritis, inflammatory bowel disease, and multiple sclerosis. 
IL-23R and Aging: Key Findings
The research team analyzed blood samples from 40 men and 40 women aged 20 to 90, finding that IL-23R levels increased with age. Preclinical models further revealed that IL-23R levels correlated with senescence markers in aged organs, particularly in the kidneys.
Using five different senotherapeutics—drugs designed to eliminate senescent cells—the researchers showed that these therapies reduced circulating IL-23R levels. These drugs targeted genes and proteins heavily expressed in senescent cells, significantly reducing inflammatory mediators like IL-23R.
“By removing senescent cells, we can decrease inflammatory signals such as IL-23R in tissues and circulation, reshaping the inflammatory landscape of the body,” says lead author Chase Carver, Ph.D.
Implications for Aging and Future Research
IL-23R’s link to inflammation and senescence highlights its potential as a biomarker for aging-related diseases. The researchers aim to study how circulating IL-23R influences inflammatory signaling and drives disease progression.
Ongoing collaborations will explore whether other interventions, such as exercise or additional senotherapeutic approaches, can further reduce IL-23R levels in humans. This work could pave the way for new clinical applications in aging and inflammatory disease management.
