Mitrix Bio CEO and Founder on mitochondrial degradation – and how it drives aging and lifespan.
DISCLOSURE: Longevity.Technology (a brand of First Longevity Limited) has been contracted by the company mentioned in this article to support its current funding round. Qualifying investors can find out more via the Longevity.Technology investment portal.
Mitochondrial dysfunction has been implicated in dozens of chronic diseases from Alzheimer’s to CVD and from frailty to immune senescence. Californian longevity biotech start-up Mitrix Bio is targeting that dysfunction with its novel mitlets platform.
Longevity.Technology: To tackle something, you have to understand it. We sat down with Mitrix Bio CEO and founder Tom Benson to get the lowdown on mitochondria, mitochondrial dysfunction and the mitochondrial cycle. It turns out that when it comes to mitochondrial replication, sometimes slow and steady really does win the longevity race.
Tom Benson on…
The fine print
The normal textbook view of mitochondria that you will see, is that they are organelles, the powerhouse of the cell and that the cell can create new ones whenever it needs – and that’s as far as it goes. We are finding out that the reality is a hundred times more sophisticated than that. Mitochondria don’t just sit in cells – in fact, they are transferring constantly between cells and inside the tissue, and being loaned and transferred by stem cells. Based on this we’ve developed a theory called The Mitochondrial Cycle of the Body; this is based on the latest research that shows, we think, that there is a significant storehouse of fresh, young, unused mitochondrial DNA, stored probably in bone marrow and stem cells, that is being rationed to the peripheral tissue.
In the course of day-to-day life, escaping from predators and normal animal activity, those external mitochondria are getting burned out, and so, in order to extend lifespan, the body is providing fresh replacement mitochondria – that’s the Mitochondrial Cycle.
How mitochondrial DNA degradation drives aging
The mitochondrial cycle has to continually supplement the mitochondrial DNA out in the stressed tissues, which are burning out their mitochondrial DNA. But why is this burn out happening? Why doesn’t a clean replication just happen instead?
Looking at the latest research, including some brilliant papers that have come out in the last few months, it all comes down to how the mitochondria are being replicated. If the replication happens in a stressful situation – running from a predator, being under a lot of stress of work – then your mitochondria replicate very quickly in order to produce quick results, but the replication isn’t very accurate and the DNA can acquire errors. It’s a sloppy replication, and while it can be important for survival, it doesn’t lead to long life.
Over the course of our lives – 80 or 90 years – that mitochondrial DNA degradation becomes unstoppable, like the tide flowing out. The body can no longer run on its reserves; it tries to manage the inventory, but it just keeps running out. Mitochondrial DNA runs out and we run out of energy – we start to age rapidly and succumb to disease, or just die.
Mitlets are mitochondria that are encased in an extracellular vesicle and used to transport fresh mitochondria back and forth in different tissues. As well as a system for recycling mitochondria, we think mitlets are the body’s number one way of distributing fresh mitochondria to the tissues. If there are 100 billion platelets created per day in the average human body, and those platelets are releasing 5 mitochondria in vesicles at the end of their lifespan, that means the body is supplemented with 500 billion new mitochondria every day.
Stay tuned for more from Tom Benson next week when we talk epigenetics and David and Goliath.
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