Protein mimics the effect of exercise and strengthens bones

According to the head of the work, Professor Xu Aimin, osteoporosis and age-related bone loss affect millions of people around the world. Elderly and bedridden patients are especially vulnerable, for whom fractures often mean loss of independence. At the same time, most of the existing prevention methods are directly related to movement and physical activity — something that is not available to everyone.

As we age, bones become more brittle, and fat accumulates in the bone marrow. This is due to the fact that mesenchymal stem cells are increasingly turning not into bone tissue, but into fat cells. Such a shift gradually weakens the bone structure and triggers a vicious circle of destruction that is difficult to stop with traditional methods.

In experiments on mice and using human stem cells, the researchers showed that Piezo1 works as an exercise sensor. When protein is activated, for example, during movement, it reduces the formation of fat in the bone marrow and stimulates the growth of new bone tissue. If Piezo1 is absent or does not work, the cells begin to accumulate fat, and bone loss accelerates.

Additionally, the scientists found that when Piezo1 is disrupted, the production of inflammatory signals increases, which further interfere with bone formation. Blocking these signals partially restores bone health, which confirms the key role of the mechanism found.

The authors of the study believe that their work paves the way for the creation of so—called exercise mimetics, drugs that will activate the Piezo1 pathway without the need for physical exertion. Such medications can be an important solution for the elderly, patients with chronic illnesses, injuries, or prolonged bed rest.

The research team is now focused on translating these findings into clinical practice. In the future, new approaches can not only slow down bone loss, but also significantly reduce the risk of fractures, improving the quality of life of an aging population.