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Scientists Use MoS2 “Nanoflowers” to Boost Mitochondria and Recharge Aging Cells

Scientists Use MoS2 “Nanoflowers” to Boost Mitochondria and Recharge Aging Cells

Researchers developed MoS2 "nanoflowers" that, when introduced into mesenchymal stem cells, stimulate mitochondrial biogenesis and double mitochondrial production in vitro. Enhanced stem cells transferred healthy mitochondria to damaged cells, restoring respiration and metabolic function. Vascular smooth muscle cells that received donor mitochondria showed improved energy capacity and transcriptome changes. Animal studies are planned to evaluate safety and efficacy before any human applications.

Researchers Stimulate Mitochondrial Biogenesis to Restore Cell Function

Cells rely on mitochondria—their energy-producing organelles—to power essential functions. When mitochondria become damaged through aging, oxidative stress, disease, or toxic exposures, cells lose energy and can malfunction, contributing to neurodegenerative, cardiovascular and metabolic disorders. A team led by biomedical engineer Akhilesh Gaharwar at Texas A&M University has developed a laboratory technique that stimulates donor stem cells to produce many more mitochondria and then transfer those healthy organelles to damaged cells.

What the Team Did

The researchers synthesized flower-like nanostructures from molybdenum disulfide (MoS2)—so-called "nanoflowers"—and introduced them into human mesenchymal stem cells (MSCs). MSCs are commonly used in regenerative research because they promote repair, have immunomodulatory properties, and consume relatively little energy, making them suitable donors for organelle transfer.

Exposing MSCs to the MoS2 nanoflowers activated intracellular pathways that promote mitochondrial biogenesis. In vitro experiments showed treated MSCs produced up to twice as many mitochondria as untreated cells. When these enhanced donor cells were co-cultured with cells that had impaired mitochondria, the excess mitochondria moved into recipient cells through specialized intercellular conduits and restored cellular respiration and metabolic activity.

Functional Improvements and Transcriptome Effects

Beyond basic energy restoration, the team tested vascular smooth muscle cells—cells that line blood vessels and require high energy for contraction and blood-pressure regulation. After receiving mitochondria from the enhanced MSCs, the smooth muscle cells displayed improved respiration and metabolic markers. The researchers also observed changes consistent with alterations in the cells' transcriptome, suggesting the mitochondrial transfer influenced gene expression patterns linked to metabolic function.

"Our MoS2 nanoflower-based strategy offers a broadly applicable platform for pathologies requiring mitochondrial repair and replacement," Gaharwar and colleagues wrote in their PNAS report. "By enhancing mitochondrial transfer and promoting mitochondrial biogenesis, this nanomaterial approach holds promise as a therapeutic tool for managing mitochondrial dysfunction."

Limitations and Next Steps

All experiments to date have been conducted in vitro (in cell culture). The approach has not yet been tested in living animals or humans. The research team plans animal studies to assess safety, biodistribution, efficacy and potential side effects before considering clinical translation. The researchers note that patients in early stages of degenerative diseases are the most likely initial beneficiaries if the method proves safe and effective in vivo.

Implications

If subsequent animal and human studies confirm these findings, the technique could open new avenues for treating conditions associated with mitochondrial dysfunction and possibly for interventions that slow cellular aspects of biological aging. However, clinical relevance depends on successful demonstration of safety and durable benefit in living organisms.

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