A way to assess the risk of early death using two parameters has identified

The activity of two genes — CDKN1A and LGALS3 — may serve as an indicator of accelerated aging and an increased risk of early death. This is the conclusion reached by scientists at Harvard Medical School after analyzing more than 11,000 tissue samples from humans, macaques, rats, and mice. The results of the study were published in the journal Nature.

The researchers sought molecular signs of aging that manifest similarly across different species and in various cell types. Ultimately, they identified a group of genes whose activity changes predictably with age. Particular attention was drawn to CDKN1A and LGALS3: the proteins associated with them turned out to be closely linked to the development of several chronic diseases simultaneously and a higher risk of premature death.

The work also showed that aging is associated with multiple biological processes at once. Among them are chronic inflammation, accumulation of DNA damage, decreased efficiency of cellular metabolism, and gradual cellular "exhaustion."

To more precisely track these changes, the scientists developed special "aging clocks" — an algorithm that assesses the biological age of various cells and tissues. The system makes it possible to determine which processes in the body are aging faster than others.

Using the new tool, the researchers found that chronic diseases accelerate aging primarily by intensifying inflammation. At the same time, certain interventions can slow this process. Experiments on animals and cell cultures demonstrated the positive effects of caloric restriction, as well as a number of cellular rejuvenation and reprogramming methods.

According to the authors of the study, the discovered biomarkers could become the basis for new methods of assessing biological age and predicting health risks. In the future, this could help doctors identify individuals with accelerated aging and develop more effective strategies for preventing age-related diseases.