Mitrix Bio Leveraging Mitochondria Transfer for Antiaging

Mitochondrial dysfunction is implicated in dozens of age- related diseases, including Alzheimer’s, retinal disease, liver dysfunction, immune senescence, and more.

Mitrix Bio has pioneered a new way of addressing these diseases, using young bioreactor-grown mitochondria encased in vesicles, which they call Mitlets.

Mitochondrial energy declines as we age, causing a wide array of chronic diseases. Scientists have tried to fix this problem with drugs that bolster membranes, reduce excess fusion, and increase mitophagy. However, these have not translated well into humans because the heart of the problem is the mitochondrial genetic code (mtDNA), not easily addressed by traditional drugs.

At Mitrix they have created an array of technologies and infrastructure, aiming to reverse mitochondrial mtDNA degeneration on a global scale.

Research over the last decade shows that Mitochondria is transferred within the body millions of times a second. The body wants to conserve Mitochondria. Researchers in the past decade have found that mitochondria don’t just sit in cells, but in fact constantly transfer around the body. Everyday, hundreds of billions are transferred through the bloodstream, brain, heart, and other organs, in order to supplement cells in need. Many of these mobile mitochondria are encased in extracellular vesicles – what Mitrix Bio calls Mitlets.

Mitlets are a natural fountain of youth within the body, used to balance and preserve healthy cellular energetics; an extraordinary evolutionary adaptation to increase survival and longevity of species. They can be isolated, transplanted, grown, and manipulated, presenting broad potential for disease-modifying treatments.

Mitrix Bio only has had some level of seed funding but they are working with Stanford University and other researchers.

Mitochondria is Damaged as We Age

Mitrix Mitochondria Transplants

The Mitrix bioreactor grows ‘young” mitochondria in large quantities, then wraps them in a special coating, with receptors to target specific organs. The goal is to produce bioreactor-grown mitochondria on an industrial scale, a “tool kit” of many different types of mitochondria that can be used by clinicians to regenerate different organs, sufficient to supplement every human being over the age of 55 and reduce severity of a wide array of diseases.

Mice and Rats Are Not Mitochondrially Limited – Problem Difference With Humans

2020 Harvesting, Injecting and Deliverying Mitochondria to Tissue in Rats

Targeted delivery of mitochondria to the liver in rats

Mitochondrial damage is commonly involved in liver injury. We have previously shown that normal mitochondria can be coated with a carrier protein to form complexes that are specifically taken up by liver cells in culture. The aim of the current study was to determine whether mitochondrial complexes could be specifically delivered to the livers of living rats by intravenous injection.

Mitochondria were harvested from fresh mouse liver, mixed with an asialoglycoprotein-based carrier, asialoorosomucoid-polylysine (AsOR-PL), and purified to form complexes. To facilitate the release of internalized mitochondria from endosomes, an endosomolytic peptide, listeriolysin O (LLO), was coupled to AsOR to form AsOR-LLO.

Results: Calculations revealed that approximately 27% of the total injected mitochondria was detected in the liver, while less than 2% was found in spleen, and < 1% in lungs. Conclusions: Targetable mitochondrial complexes can be delivered to rat liver, and the efficiency of that process is greatly enhanced by co-injection of a targetable endosomal release agent, AsOR-LLO.

19 thoughts on “Mitrix Bio Leveraging Mitochondria Transfer for Antiaging”

  1. Some saved info..

    Unified Theory of Aging:

    Nitric oxide controls and regulates

    1) Telomerase activity
    2) Mitochondrial biogenesis and function
    3) Mobilization of resident stem cells.

    Nitric oxide (NO) controls and regulates Mitochondrial:

    ATP Synthesis
    Reactive oxygen species
    Cell signalling
    Apoptosis (cell cycle)
    Biogenesis
    Metabolism/Bioenergetics

    If you want to live longer and better, your body must be able to produce nitric oxide.

    By your 40s, the body only produces 50% NO as when in your 20s. Hence wrinkles, thickening arteries, plaque buildup etc. When 60+, NO production reduces to 15%.

    There are two nitric oxide production pathways:
    1) Oxidation of L-Arginine (NOS)
    2) Nitrate>Nitrite>Nitric Oxide

    Each pathway provides about 50% of total NO production.

    L-Arginine to NO produces L-citrulline which recycles back to L-Arginine.

    Watermelon (especially the white core of the peel) is a good source of L-citrulline.

    Nitrate is inert in humans. Must be reduced to nitrite by bacteria on your tongue, gets there via saliva. (so don’t use antibacterial mouthwash..)

    Best sources of nitrates are spinach, celery and beets.

    • Watermelon (especially the white core of the peel) is a bad source of L-citrulline.
      use L-citrulline powder

      worst sources of nitrates are spinach, celery and beets – oxalates

      Best sources of nitrates are meats

  2. I recall seeing (a few years ago now) results that older people benefited from receiving ‘young blood’. I wonder if this is why.

    • HI Eric,

      Correct, Blood is jam-packed with transplantation-ready mitochondria. If you get young blood, you are getting a shot of young mitochondria.

      Parabiosis is a mitochondrial treatment.

    • No, they finally determined that it was simply a matter of senescent cells excreting toxic substances that ended up circulating in the blood, poisoning you. The ‘young blood’ just diluted them.

      You actually get just as much benefit from donating some plasma and having the volume replaced with a simple IV solution.

      Naturally, I can’t do that, because the blood/plasma industry is insane on the topic of cancer.

      • Interesting.

        I have hereditary hemochromatosis, and the treatment for that is phlebotomy. Too much iron in the blood, so regularly remove blood, thereby reducing the iron level. I never thought of it as a life extension approach.

        • Yeah, actually that is a recognized life extension treatment. Lower blood iron levels are hypothesized to be one of the reasons women are more resistant to brain aging. See this report:

          https://www.lifeextension.com/magazine/2012/3/excess-iron-brain-degeneration?srsltid=AfmBOoqAP_mBMveGTa4P0Aj7ONZ-k0Osf_piMHbniIZVjIpumvXl-GgJ

          Lowering my blood iron levels, (Which weren’t clinically high, but were high for purposes of longevity.) was why I used to routinely donate blood. I’d still be doing it, if it weren’t for the blood industry’s clinical grade paranoia concerning lymphoma. (Like I’d still be alive over a decade later if I hadn’t been completely cured.) I’m not permitted to donate plasma, either, which is doubly irrational.

          • Thanks Brett.

            With hemochromatosis, the blood drawn during phlebotomy is essentially thrown away. No worries about donating. You may want to look into that.

            • Without a diagnosis of hemochromatosis, trying getting that done affordably… It’s not like you can show up at the bloodmobile and ask them to just take your blood and toss it.

              Well, not if you’re a cancer survivor, anyway. If I were merely mainlining heroin I could…

              I suppose I could do it self help, but I suspect it would freak out my wife.

  3. Some quotes from the video:

    We are not gonna squeeze mitochondria from teenageres. It wouldn’t be popular…

    • There’s no particular reason why mitochondria would be difficult to manufacture in ton lot quantities. It’s true that they can’t grow in a cell free media, because they’re not genetically complete, but in principle you could grow human mitochondria in any eukaryote cell culture with just a bit of genetic engineering to get the nuclear mitochondrial genes to match.

      Extracting them from teens would be pointless. Maybe liposuction patients might make sense…

  4. The article is too “flashy” . There is no need of a special “coating” to hone extracellular vesicles towards the liver. It is one of the most metabolically active organs and will soak the mitochondria by default. A couple of years ago it was shown that such mito-transplant can enhance many organs and tissues in-vivo and in-vitro. The novel part here seems to be the “bio-reactor” part. However, the “results” part is the one that is mostly lacking.

    There is, at least at first glance, a winning strategy. Modify some tissues to produce and shed mitochondria in great quantities. Make research to prove clinical effect, and donor-host compatibility in humans. So fart it seems that mitochondria, unlike cells to be quiet compatible. Find way to concentrate and freeze those vesicles, if needed matched by immune profiles.

    profit.

    Mito therapy seems like a good candidate for a cash-cow. Everybody above certain age (50, 60 ?) will definitely benefit from it , and if th e cost is under 10k a year per person, it would be like a must have for millions.

    Not to mention that such a treatment can help, if not eliminate many classes of mitochondrial disease . Genetic defects and such..

  5. More on antiaging research:

    “A study published in Nature looked into how to uncover and manipulate the molecular processes of aging. More specifically, researchers investigated a pro-inflammatory protein called interleukin-11, or IL-11. Levels of IL-11 increase in the human body as we get older and this contributes to higher levels of inflammation, which has been shown to increase your risk for a number of issues, including cancer, type 2 diabetes, heart disease, and dementia. This is why researchers believe that this protein may play a significant role in the pace of aging.”

    See:

    https://www.yahoo.com/news/scientists-discover-anti-aging-therapy-123000186.html

    • This was super interesting report on a study suppressing IL-11 receptor in mice, both via gene editing and also via a drug (there are human IL-11 suppressors in approval process). Up to 50% longevity increase when started in middle age mice and dramatically reduced frailty. If it works in humans that is like 80=>100yr life expectancy.

      https://youtu.be/9KrI1AQUhrg?t=54

  6. Also there must be a native mechanism for this. Considering mitochondria are passed down mother to fetus for essentially since the beginning of time. That’s a long time to have genetic damage. If it’s this much on an issue over a single animal lifetime we should all be goo by now.

    • It’s pretty simple: Every living person goes through a single cell bottleneck, where if that fertilized egg cell isn’t virtually 100% functional, there’s a miscarriage. Most pregnancies end so early on account of this that they’re never even noticed.

      That quality control step eliminates an awful lot of harmful mutations. For the most part mitochondrial mutation has to start over from scratch with each new organism, from a known good set of mitochondria.

    • Unfortunately, once you get a non-energy generating mutant mitochondrion in a cell, it has a bit of a reproductive advantage over the ones that are still generating energy, under some circumstances. It’s all down to the balance between garbage collection of mutants, vs normal mitochondria damaged by the free radicals generated by normal functioning. At low levels of operation clean up of mutants dominates, at high levels, the mutants have a selective advantage because they don’t accumulate damage.

      Muscle tissue are particularly prone to this, because they’re working their mitochondria hard; Germ line cells have their mitochondria down-regulated just to avoid this fate.

      It doesn’t seem like a protocol like that, even if it worked, would rescue cells in that situation, since there are no functional mitochondria to favor. Mitochondrial transplants could rescue them.

      But I am seriously considering trying that protocol anyway.

      You might find this article interesting, it goes into great detail concerning these selective pressures:

      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9802247/

      • “Turbuckle” addresses this issue. He says his protocol deals with this issue because it eliminates the mDNA of the defective mitochondria. It also fixes the epigenetic issues as well.

        In any case, yamanaka factor reprogramming of cells also restores the mitochondria to young status. Although you do not want to use the yamanaka factors on yourself. You can extract cells from you body, convert them to stem cells (which also rejuvenates them) and extract the youthful mitochondria from them to use in this procedure. The rest of the process looks like it could possibly be done in a home lab, thus bypassing Big Pharma.

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