Aggf1 Delays Endothelial Cellular Senescence Through The Tgfb3-Tak1-AMPK Signaling Axis
Our blood vessels are lined with special cells called endothelial cells, and as we age, these cells can undergo a process called senescence, essentially becoming “old” and dysfunctional. This cellular aging contributes significantly to various age-related diseases affecting our blood vessels. Recent research has shed light on a protein called AGGF1 and its crucial role in keeping these endothelial cells young and healthy.
Scientists found that when endothelial cells become senescent, the levels of AGGF1 decrease. Conversely, increasing AGGF1 levels can prevent these cells from aging, while reducing AGGF1 accelerates the aging process.
So, how does AGGF1 achieve this? The studies revealed that AGGF1 kickstarts a specific communication pathway within the cells. It does this by increasing the production of a molecule called TGFB3, which then activates two other important proteins, TAK1 and AMPK. This activated pathway is vital because it helps to prevent excessive fragmentation of mitochondria, the powerhouses of our cells. By maintaining healthy mitochondrial shape and function, this pathway effectively delays cellular senescence.
In essence, this research highlights AGGF1 as a key player in controlling cell metabolism and preventing the aging of endothelial cells, primarily by ensuring our cellular power plants, the mitochondria, remain in good working order.
Source: link to paper