Mitochondrial Dysfunction Drives Age-Related Degeneration Of The Thoracic Aorta
As we age, our bodies undergo various changes, and one crucial area is the health of our arteries. The aorta, the body’s largest artery, can become stiff and less flexible over time, increasing the risk of serious conditions like high blood pressure and aneurysms. Recent research sheds light on a key player in this age-related decline: the mitochondria. These tiny powerhouses within our cells are responsible for generating energy. When they don’t function properly, a state known as mitochondrial dysfunction, it appears to drive the aging process in the aorta.
Scientists investigated this connection by studying aged mice. They found that treating these mice with a special compound designed to target and improve mitochondrial function, called elamipretide, had remarkable effects. The treatment helped restore the mitochondria’s ability to produce energy efficiently and also reduced signs of inflammation and damage to the aorta’s elastic fibers, which are crucial for its flexibility. Furthermore, the treatment influenced the activity of genes in the aorta, reducing those linked to cellular aging and inflammation.
These findings suggest that the health of our mitochondria is directly linked to how our arteries age. By understanding and potentially targeting mitochondrial function, we may open new avenues for developing therapies to maintain a healthy cardiovascular system as we get older.
Source: link to paper