GUANGZHOU -- Chinese researchers have recently made a breakthrough by developing a novel and highly efficient mitochondrial capsule transplantation therapy, achieving the safe and efficient transplantation of healthy mitochondria into cells and tissues for the first time. This new therapy can significantly alleviate symptoms of severe diseases such as Parkinson's disease.

According to the study published on Wednesday in the journal Cell, the therapy proposes a brand-new strategy in the field of regenerative medicine, shedding fresh light on intervention in refractory diseases caused by mitochondrial dysfunction, such as mitochondrial genetic diseases and neuron degenerative disorders.

Mitochondria are organelles that refer to specialized subunits with specific functions in cells. Mitochondria function like power plants in cells, continuously converting nutrients into energy for life activities. They are also the only organelles in human cells that possess their own genome.

Mutations in mitochondrial genes can lead to severe genetic diseases, affecting more than 1 in 5,000 people worldwide. However, doctors have only been able to manage symptoms without fundamentally repairing the malfunctioning mitochondria. Their dysfunction is a significant contributing factor to aging and various neuron degenerative and metabolic diseases, including Parkinson's disease, Alzheimer's disease and diabetes.

A research team from the Guangzhou Institutes of Biomedicine and Health under the Chinese Academy of Sciences, Guangzhou Medical University and other institutions, utilized membrane vesicles from red blood cells as "capsules" to encapsulate healthy mitochondria, creating mitochondrial capsules with a diameter of one-thousandth of a millimeter.

The study notes that these capsules not only protect the mitochondria, but also help them pass through a cell's defense system, successfully enter the cell interior, and fuse with the cell's own mitochondria to achieve long-term survival.

The study found that the delivery efficiency of naked mitochondria was less than 5 percent, whereas the new therapy demonstrated high delivery efficiency, with roughly 80 percent of target cells successfully accepting the new mitochondria.

More importantly, once these foreign mitochondria enter the cell, they do not exist in isolation. Instead, they actively integrate with the cell's existing mitochondrial network, continuously functioning in the cell to compensate for metabolic disorders and functional deficiencies.

The research team also conducted tests on cells from patients with various mitochondrial DNA mutations. These cells contained both healthy and malfunctioning mitochondria at the same time. After successful transplantation of healthy mitochondria, the proportion of malfunctioning mitochondria in the cells significantly decreased. The previously malfunctioning cellular energy metabolism was rapidly restored, and genetic defects were compensated.

The study also established multiple disease animal models, including Parkinson's disease, Leigh syndrome and mitochondrial DNA deletion syndrome.

In the Parkinson's disease mouse model, after delivering mitochondrial capsules to the affected brain regions, the therapy effectively prevented continuous neuronal death, restored normal mitochondrial function in the brain region, and significantly improved the motor abilities of the model mice, nearly restoring them to normal levels.

In mouse models for mitochondrial genetic diseases, the new therapy significantly extended the lifespan of the diseased mice and rescued multiple organ failures.

According to the study, it may be possible to use healthy organelles, including mitochondria, as a form of medicine, and directly deliver them into patients to repair the functioning of diseased tissues and organs.