How Exercise Reduces DEAF1 Levels to Slow Muscle Aging, Scientists Reveal

Unveiling the Cellular Impact of Exercise

According to НВ — Техно: A team of international researchers has identified the biological process through which physical exercise delays muscle aging and enhances regenerative capacity. Conducted by experts from Duke-NUS Medical School, Singapore General Hospital, and Cardiff University, the study found that exercise triggers proteins that suppress the DEAF1 gene. This suppression helps restore balance in the mTORC1 signaling pathway and promotes the removal of damaged proteins within muscle cells.

The Role of Physical Activity in Muscle Health

Muscle mass and strength typically begin to decline around middle age, a change linked to increasing DEAF1 gene expression in muscle tissue. Under normal conditions, FOXO proteins regulate DEAF1 levels, but when DEAF1 becomes overexpressed, it leads to excessive activation of mTORC1, which inhibits muscle self-repair processes. Engaging in physical exercise lowers DEAF1 expression and normalizes mTORC1 activity, enabling muscle cells to clear out damaged proteins more effectively.

Experiments involving fruit flies and aged mice confirmed these findings: elevated DEAF1 weakened muscle strength, while reducing DEAF1 restored it. However, in cases where DEAF1 levels are critically high and FOXO protection is diminished, exercise alone may not fully recover muscle function. Additionally, DEAF1 influences muscle stem cells responsible for regeneration after injury.

These insights emphasize the crucial role of regular physical activity in preserving muscle health, especially as people grow older.

The researchers hope that understanding these molecular pathways will pave the way for new treatments aimed at improving muscle recovery in individuals with limited ability to exercise. Such advancements could significantly enhance quality of life for those experiencing age-related muscle decline or disease-related muscle damage.

In addition to the findings on DEAF1, recent research has also highlighted the role of ion channels in muscle weakness associated with aging. Understanding how NaV1.4 and ClC-1 channels impact muscle function can provide further insights into the complexities of muscle health as we age, offering potential avenues for targeted therapies.