Juan Carlos Izpisua Belmonte, co-founder of Altos Labs, proposes that aging and many diseases may stem from a loss of cellular identity. He theorizes that restoring this identity could allow cells to function more like they did in youth, potentially offering a comprehensive approach to combating age-related decline and illness.

Belmonte's concept centers on the idea that during embryonic development, the body's genes organize to create over 200 distinct cell types, a process akin to individuals developing a personal identity. Over time, however, this cellular identity can be compromised by factors such as inflammation, environmental exposures like pollutants, and lifestyle choices including poor diet, lack of exercise, and smoking. The accumulation of these effects, according to Belmonte and other developmental experts, is a significant driver of aging and disease.

Altos Labs was founded to explore this hypothesis. Instead of completely reverting adult cells to an embryonic state, as demonstrated by Shinya Yamanaka, Belmonte investigated whether partial reprogramming could be sufficient to guide cells back to their proper developmental pathways and restore youthful function and identity. In 2025, he reported success in both lab-grown human cells and in mice.

Treatments involving Yamanaka's genetic factors partially reprogrammed and rejuvenated cells in various organs of older mice, including the kidneys, liver, and intestines. Skin cells, for instance, regained enhanced regenerative and wound-healing capabilities. Belmonte believes that addressing cellular identity issues could allow for a more unified strategy against a wide range of diseases, rather than addressing each one individually.

The next phase of research involves transplantation studies. Scientists at Altos are beginning to assess whether partially reprogrammed cells can rejuvenate and redirect aging cells in multiple organs back to a more functional, youthful state when transplanted into older animals.

For human applications, Belmonte suggests initial studies could focus on increasing the availability of organs for transplant. Younger organs generally yield better outcomes for recipients. His previous work at the Salk Institute demonstrated that reprogramming kidneys from older animals enabled them to function as well as those from younger donors, extending the lifespan of the mouse recipients.

"It's proof that independently of disease, or of the problem, re-establishing cell identity could have a major effect in the progression of any disease," Belmonte stated. His team has reported similar success in reprogramming diseased cells across nearly three dozen conditions in mice.

However, Belmonte cautions that findings in mice do not directly translate to humans and that partial reprogramming as a method to slow aging requires further investigation. He expressed optimism that if transplant results are replicated in humans, it could lead to the use of more organs from older donors, marking a significant advancement in cellular rejuvenation research. The ultimate goal, he noted, is to mimic the cellular state of early life, though whether this can prevent aging remains an open question.