Mitochondria From a Woman's Leg Were Injected Into Her Eyes in World First

When the batteries in a television remote run flat, you may find yourself searching through a desk clock for replacements.

We do not usually think of the human body in those terms. Yet scientists are starting to investigate whether something similar might be possible at the cellular scale.

In animal experiments, researchers have tested mitochondrial transplants - transferring the microscopic structures that provide cells with energy into injured tissue - in an effort to give failing cells a fresh power source.

For the first time, they have now attempted this by injecting mitochondria into a human eye.

In a young woman with profound sight loss, doctors isolated mitochondria from cells obtained through a leg biopsy, then injected them straight into the vitreous fluid in both eyes.

Encouragingly, no harmful effects occurred. According to a preprint case report led by neuroscientist David Putrino at the Icahn School of Medicine at Mount Sinai and posted on Research Square, this is an important early sign that the procedure itself may be safe enough for further study.

More intriguingly, although the patient's vision did not return, there may also have been a positive effect.

How mitochondria could support damaged retinal cells

Mitochondria are tiny cellular batteries, converting food and oxygen into the usable energy cells need to carry out their functions.

Certain cells depend particularly heavily on mitochondrial energy. These include retinal ganglion cells, the neurons that carry visual signals from the retina to the brain. Putrino and colleagues say these cells rank among those with the greatest energy requirements in the central nervous system.

If the supply of blood and oxygen is cut off, mitochondria may be damaged. That damage can, in turn, contribute to the sequence of events that destroys retinal ganglion cells.

The aim is not for transplanted mitochondria to bring dead neurons back to life. Rather, healthy mitochondria could potentially restore energy generation in retinal ganglion cells that remain alive and might still be saved.

Animal research has found that transplanted mitochondria can be absorbed by retinal cells, and may even help some retinal ganglion cells survive following injury.

For one young woman, this prospect provided a glimmer of hope after more established treatments had produced no benefit.

Mitochondrial transplant in a patient with severe sight loss

At the age of 26, she experienced a major brain haemorrhage and was not taken to hospital until an estimated 18 hours afterwards. Emergency surgery saved her life, but the extended deprivation of blood and oxygen to her optic nerves left her almost entirely blind in both eyes.

Brain and eye imaging showing damage to the patient's optic nerves and retinal ganglion cells before the mitochondrial transplant. (Putrino et al., Research Square, 2026)

Eight weeks later, visible atrophy had developed in her optic nerves. At roughly three months, when treatment took place, her severe visual impairment had not improved in any meaningful way.

That did not necessarily mean there was no remaining potential. Scans revealed that the retinal nerve-fibre and ganglion-cell layers, though severely thinned, had not vanished completely. Measurements of brain activity also indicated that some visual information was still reaching the visual cortex.

A mitochondrial transplant might therefore have been capable of restoring energy to the cells that remained.

In transplantation procedures, the patient's own biological material is generally the safest option for reducing the chance of an immune reaction. Doctors therefore collected a biopsy from her thigh muscle and processed it to isolate tens of millions of mitochondria from its cells.

While still fresh, the mitochondria were injected into the gel-like fluid of each eye.

Within days, there was a change.

What happened after the eye injections

Over the 71 days before treatment, doctors recorded 45 measurements of how her pupils responded to light. None showed a normal response.

Only a few days after the injections, both pupils began to display some normal responses. Moreover, during three separate brain-recording sessions conducted 3, 44, and 45 days after treatment, researchers observed an organised response in the visual cortex.

This did not indicate that her sight had been restored. Her visual acuity essentially remained limited to light perception and did not change measurably after treatment.

The pupillary responses were not permanent either. The final normal response in the left eye was recorded on day 11, whereas the right eye continued to show occasional normal responses until day 39.

There are substantial limitations to consider. This involved only one patient and had no controls. There was no direct evidence that the transplanted mitochondria entered her retinal ganglion cells. Finally, the authors stress that this case cannot establish causation.

What is known is that the procedure caused no serious adverse effects, and her body did not produce a dangerous immune reaction.

Related: First-of-Its-Kind Treatment Boosts Vision in Human Trial, Scientists Report

The research nevertheless provides a clear route for future study. Because the observed changes were temporary, one possibility is that damaged cells may require repeated doses of healthy mitochondria to maintain any benefit.

Before that can be explored, however, researchers must establish clearly whether the transplanted mitochondria caused the changes.

If they did, using cellular batteries from elsewhere in a patient's own body could eventually provide a new means of rescuing damaged eye cells.

"Now that we've shown that we can do this safely," Putrino told Nature, "we are working with the FDA to come up with a protocol for repeated serial mitochondrial injections."

The findings are available on Research Square.

This article was fact-checked and edited by Fiona MacDonald. Although we take pride in our process, we are only human. If you spot an error, please let us know.