Artificial mitochondrial transplantation rejuvenates mesenchymal stromal cells, reducing senescence and enhancing anti-inflammatory effects. By transferring healthy mitochondria, aged cells regain energy metabolism, diminish oxidative stress, and improve insulin sensitivity, presenting a promising tool for regenerative therapies targeting ageing and chronic inflammation.
October 2024 – Science Direct
Key Takeaways
- Healthy mitochondria reverse cellular ageing and reduce senescence: Transferring functional mitochondria to ageing stromal cells restores their vitality by reducing cellular senescence markers like beta-galactosidase activity and apoptosis-related proteins. This rejuvenation process helps the cells regain their functional capacity, offering a promising approach to counteract the biological effects of ageing
- Rejuvenated cells exhibit improved energy metabolism and reduced oxidative stress: Introducing healthy mitochondria improves oxygen consumption and ATP production in impaired cells, restoring their energy balance. This also reduces the harmful effects of oxidative stress, a significant contributor to ageing, by enhancing antioxidant defences and mitochondrial quality
- Mitochondria transfer enhances insulin sensitivity and cellular repair: Rejuvenated cells demonstrate improved insulin signalling, including enhanced activity of critical pathways such as the PI3K-Akt pathway. These changes improve the cells’ ability to respond to metabolic cues, aiding tissue repair and reducing the risk of metabolic dysfunctions commonly associated with ageing
- The anti-inflammatory properties of stromal cells are significantly enhanced after mitochondrial transfer, as seen in their ability to suppress pro-inflammatory cytokines. This improvement positions these rejuvenated cells as valuable assets for therapies targeting inflammation-related ageing diseases
Read the article at: Bourebaba, Lynda, et al. “Artificial mitochondrial transplantation reverses aging of mesenchymal stromal cells and improves their immunomodulatory properties in LPS-induced synoviocytes inflammation.” BBA – Molecular Cell Research, vol. 1871, 2024, doi:10.1016/j.bbamcr.2024.119806.