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Research has demonstrated that transferring mitochondria from a patient’s normal skeletal muscle to damaged, ischemic cardiac tissue can enhance ventricular function, increase energy generation, and recover heart muscle.
Heart surgeons led by Sitaram Emani, MD, have been investigating it as a means of assisting infants with congenital heart disease and ischemia-reperfusion injury in weaning off of ECMO (extracorporeal membrane oxygenation) since James McCully, Ph.D., pioneered preclinical work on the subject at Boston infants’s Hospital almost ten years ago.
Researchers discovered that adding mitochondria significantly increased the likelihood of recovery. There have been sixteen pediatric autologous mitochondria transplants performed to date. Out of them, 80% were able to stop using ECMO, which is higher than the 40% historical average.
However, there has been doubt about mitochondrial transfer, partly because its mechanism of action is still unknown.
Scientists concluded that it was mitochondria entering cells, taking control, and producing all of the energy within the cell. However, the fact that the heart muscle could heal with such tiny quantities of mitochondria contradicted logic. The calculations were off.
Juan Melero-Martin, Ph.D., a researcher in the Department of Cardiac Surgery, led a study that was published in the journal Nature and discovered an unexpected explanation. The transplanted mitochondria cause the cell to engage in cellular housekeeping called autophagy, which results in the destruction of its underperforming mitochondria.
This increases the amount of mitochondria in cells, enhancing their fitness and bioenergetics. The discovery could ultimately contribute to better treatment for an array of heart ailments.
Sources:
Ruei-Zeng Lin et al. (2024). Mitochondrial transfer mediates endothelial cell engraftment through mitophagy, Nature. DOI: 10.1038/s41586-024-07340-0. https://www.nature.com/articles/s41586-024-07340-0
https://phys.org/news/2024-06-mitochondrial-heart-muscle.html
