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Engineered protein binders have enabled selective mitochondrial transplantation to diseased cells with preclinical evidence of improved neuronal survival and broad applicability across human tissues
A research team led by Dr. Botond Roska at the Institute of Molecular and Clinical Ophthalmology Basel, Switzerland, has developed a system to enable targeted delivery of healthy mitochondria to diseased cells, in a development that has advanced the prospect of precision mitochondrial therapy.
Mitochondrial dysfunction has been implicated in a wide range of conditions that remain difficult to treat, including neurodegenerative diseases such as Parkinson’s disease and Alzheimer’s disease, alongside other conditions such as optic nerve atrophy and heart failure. Although researchers have explored mitochondrial transplantation as a therapeutic strategy, conventional approaches have lacked the specificity and efficiency required to target affected cell populations.
The MitoCatch system has addressed this limitation through the use of engineered protein binders that link donor mitochondria directly to selected target cells. The platform integrates three complementary approaches:
Researchers have reported that careful adjustment of binder affinity and multivalent interactions enabled efficient and selective mitochondrial delivery across a range of human and mouse cell types.
Work led by first authors Dr. Temurkhan Ayupov and Dr. Veronica Moreno-Juan has demonstrated that the system can direct mitochondria to diverse cell populations, including neurons, retinal cells, cardiac cells, endothelial cells and immune cells.
Binder-mediated delivery increased uptake relative to untargeted approaches and transferred mitochondria have shown functional integration within recipient cells, with evidence of cytosolic exposure and participation in fusion and fission dynamics.
The investigators have also shown that the protein binders can be engineered to modulate delivery efficiency and specificity, an attribute that strengthens the system’s translational potential. In preclinical models, targeted mitochondrial transplantation improved survival of damaged neurons in vitro and retinal ganglion cells in vivo. The intervention has also proved well tolerated in animal models, with no detectable immune response under the conditions tested.
These findings have marked a significant step towards the long-standing objective to achieve cell type-specific mitochondrial transplantation. By enabling targeted delivery to the cells most affected by disease, MitoCatch has opened a route to explore mitochondrial replacement strategies across multiple indications linked to energy metabolism and cellular dysfunction.
Its demonstrated versatility across different human cell types positions the platform as a candidate foundation for precision mitochondrial medicine subsequent to regulatory approval following validation in a clinical setting.
For further reading please visit: 10.1038/s41586-026-10391-0
Lab Asia 33.2 April
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