Fight Aging!

Mitochondria are the cell's roving herd of power plants, producing chemical energy stores to power cellular processes, and mitophagy is the process by which damaged mitochondria are recycled for parts. If allowed to continue functioning and dividing like bacteria, damaged mitochondria can harm the cell - and in fact forms of damage that allow mitochondria to evade mitophagy are one of the root causes of degenerative aging. In older individuals many cells are overtaken by malfunctioning mitochondria, forcing them to operate abnormally and export damaging reactive molecules into surrounding tissues.

Here, researchers make inroads into understanding more of the mechanisms by which mitophagy operates, which may open the door to correcting failures in this process. This presents another potential avenue for treatments for aging based on mitochondrial repair to add to those that already exist and are under development.

Cardiolipins, named because they were first found in heart tissue, are a component on the inner membrane of mitochondria. When a mitochondrion is damaged, the cardiolipins move from its inner membrane to its outer membrane, where they encourage the cell to destroy the entire mitochondrion. "It's a survival process. Cells activate to get rid of bad mitochondria and consolidate good mitochondria. If this process succeeds, then the good ones can proliferate and the cells thrive."

[The newly identified part of this mechanism] turns out to be a protein called LC3. One part of LC3 binds to cardiolipin, and LC3 causes a specialized structure to form around the mitochondrion to carry it to the digestive centers of the cell. "There are so many follow-up questions. What is the process that triggers the cardiolipin to move outside the mitochondria? How does this pathway fit in with other pathways that affect onset of diseases like Parkinson's? Interestingly, two familial Parkinson's disease genes also are linked to mitochondrial removal." While this process may happen in all cells with mitochondria, it is particularly important that it functions correctly in neuronal cells because these cells do not divide and regenerate as readily as cells in other parts of the body.

"I think these findings have huge implications for brain injury patients. The mitochondrial 'eat me' signaling process could be a therapeutic target in the sense that you need a certain level of clearance of damaged mitochondria. But, on the other hand, you don't want the clearing process to go on unchecked. You must have a level of balance, which is something we could seek to achieve with medications or therapy if the body is not able to find that balance itself."

Link: http://www.sciencedaily.com/releases/2013/09/130930140518.htm