TEXAS: Researchers at Texas A&M University may have discovered a way to stop—or even reverse—the decline of cellular energy, bringing science one step closer to “recharging” aging tissues in humans.
The team’s approach targets mitochondria, the tiny “powerhouses” of cells responsible for producing energy.
By replacing old or damaged mitochondria, the researchers restored energy output and significantly improved cell health, according to a latest study published in Newsweek.
“This is an early but exciting step toward recharging aging tissues using their own biological machinery,” said study author and biomedical engineer Professor Akhilesh Gaharwar.
“If we can safely boost this natural power-sharing system, it could one day help slow or even reverse some effects of cellular aging.”
Mitochondrial decline is linked to aging, heart disease, and neurodegenerative disorders. Enhancing the body’s natural ability to replace worn-out mitochondria could combat these conditions, the team explained.
The breakthrough combines stem cells with “nanoflowers”—tiny flower-shaped nanoparticles. When stem cells are exposed to these nanomaterials, they produce twice as many mitochondria as usual.
These boosted stem cells can then transfer their extra mitochondria to nearby damaged cells, restoring energy and function.
“Our method amplifies the innate ability of stem cells to donate mitochondria,” Gaharwar said. “We’re enhancing a natural repair mechanism rather than creating a new one.”
In laboratory tests, cells rejuvenated through this technique resisted cell death even after exposure to chemotherapy drugs.
The stem cells transferred two to four times more mitochondria than untreated cells, dramatically increasing their repair efficiency.
The researchers believe this approach may be most effective in diseases where mitochondrial failure is a primary cause, such as genetic mitochondrial disorders, Parkinson’s disease, ALS, cardiomyopathies, and acute organ injuries.
It could also help mitigate age-related declines in muscle, metabolism, and tissue repair.
Unlike medications that require frequent dosing, the larger nanoparticles used in this method remain in cells longer, promoting mitochondrial creation and potentially reducing the frequency of treatments.
“The several-fold increase in efficiency was more than we could have hoped for,” said co-author John Soukar.
“It’s like giving an old electronic a new battery pack. Instead of tossing them out, we are plugging fully charged batteries from healthy cells into diseased ones.”
The next steps for the team include animal studies to confirm safety and effectiveness, with human clinical trials to follow if results remain promising.
