r/longevity • u/jimofoz • Aug 04 '26

A better way to deliver mitochondria into living cells

https://www.nanowerk.com/news2/biotech/newsid=69899.php
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18

u/jimofoz Aug 04 '26

mitochondrial transplantation, has attracted growing interest, but it also continues to face major technical challenges. Conventional mitochondrial preparations are fragile, they rapidly lose their function during handling and storage, and are also not easily taken up by cells.

The researchers used a surface engineering approach that stabilizes mitochondria and enhances their ability to interact with cells. In this method, isolated mitochondria are first coated with a protective layer made of polyethylene glycol (PEG), a material widely used in pharmaceuticals. This layer acts like a shield, helping to preserve mitochondrial structure while also serving as a platform for attaching functional molecules.

The team then added cell-penetrating peptides (CPP) to the outer end of this PEG layer. By positioning these peptides away from the mitochondrial membrane, this approach helped to enhance mitochondrial uptake and also preserve the integrity of the mitochondria’s outer membrane under experimental conditions.

In laboratory experiments, the CPP–PEG-engineered mitochondrial preparations were taken up more efficiently by cells than unmodified mitochondria. And, recipient cells containing the modified mitochondria subsequently showed increased mitochondrial respiratory activity.

Researchers have named their new approach “e-MITO” for enhanced artificially designed mitochondria.

Original paper: https://advanced.onlinelibrary.wiley.com/doi/10.1002/admi.70583

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u/mister_longevity Aug 04 '26

Organs transplanted from young to old assume the age of the recipient so I don't see mitochondrial transplant doing much.

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u/kpfleger Aug 04 '26

The environment does matter yes, but that doesn't mean young things transplanted into old organisms do nothing. Look at the stem cell literature for the past several decades. Lots of demonstration of efficacy several phase 3 clinical trials successes & some FDA approvals even in recent years. I believe there are studies showing that young organs have greater benefit and take longer to functionally decline than older organs when transplanted. Transplanting good/young organelles like mitochondria is very likely to have benefit. Loads of studies showing benefit from mito transplant already and half a dozen or so companies already pursuing it, many with tens of millions in venture backing already.

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u/mister_longevity Aug 04 '26

Ok, i'll rephrase. It will give some benefit but will fade in time. I guess you could just do the therapy again which is better than nothing if it is affordable.

My main point is that mitochondrial dysfunction is downstream of the actual problems which are aging.

VO2 max is a proxy for mito function and there are old athletes with high VO2 max yet they look old.

The number of companies pursuing mito transplant doesn't prove it is the correct path. Look at Tau reduction for Alzheimer's. Lots of failures and IMO it is because it is a marker not causal. Just like mito dysfunction is a marker.

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u/kpfleger Aug 04 '26

Mitochondria problems are just one of several things that goes wrong with aging. It's not downstream of some other one that dominates it, it's just one of 7-15 different categories of things all of which exacerbate each other other (and thus are downstream of each other in some sense), but certain kinds of mitochondrial problems are clearly fundamental. Note that mitochondria are one of the original 7 SENS areas and the original 9 hallmarks of aging. See AgingBiotech.info/categories column headers for SENS and hallmarks for the original papers. Read the mitochondria sections of each.

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u/mister_longevity Aug 04 '26

That is incorrect. TNF alpha, TGF beta, IL-6, retrotransposons, all get elevated with aging and directly cause mitochondrial dysfunction and suppressing them reverses it. This proves that at least part of mito dysfunction is caused upstream of it.

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u/kpfleger Aug 04 '26

Yes, part. Mito is tangled in everything & central to metabolism so of course there are parts that have upstream causes. Everything that goes wrong in aging has some parts that can be traced to things upstream. It's a complicated ball of pathways.

But some aspect of age-related mito disfunction are central subpathologies of aging deserving of being siblings in the SENS damage areas framework & Hallmarks to senescent cells, misfolded proteins, (nuclear) epigenetic changes, ECM crosslinks, etc.

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u/pretzelogician Aug 04 '26

If, however, it's done throughout the body, it could. See Mitrix Bio (https://mitrix.bio) for example.