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Mito-Mendelian Genetics: The New Frontier in Personalized Medicine

Mitochondria are the cell’s powerhouse, but Mito-Mendelian genetics is revealing their role as the command center for many vital processes. By understanding how mitochondrial DNA (mtDNA) interacts with nuclear DNA (nDNA), we can unlock new insights into health, disease, and personalized treatments.


Key Insights:

  • Co-evolution of Genomes: Mitochondria and the nucleus have co-evolved, influencing not only energy production but also cellular responses like immune function, proteostasis (protein homeostasis), and stress adaptation.

  • Mitochondria and the Immune System: Mitochondrial-nuclear interactions play a crucial role in regulating immune responses. Mitochondria help control inflammation and immune cell activation, making them key players in both health and disease.

  • Proteostasis: These genetic interactions are essential for maintaining protein quality control within cells, ensuring that misfolded or damaged proteins are properly managed. Disruptions in this process are linked to neurodegenerative diseases like Alzheimer's and Parkinson’s.

  • Cell Death (Apoptosis): Mitochondria also govern programmed cell death, which is critical for removing damaged cells and preventing cancer. Mito-Mendelian genetics helps us understand how these processes go awry in diseases like cancer and cardiovascular conditions.

  • Metabolic and Degenerative Disease Risk: Variations in mitochondrial and nuclear DNA influence metabolic functions, contributing to disease susceptibility, including diabetes, obesity, neurodegenerative disorders, and even certain cancers.


Mitochondria are more than energy producers—they’re central to our immunity, cell survival, and protein health. Understanding their cross-talk with nuclear DNA opens new doors for personalized medicine!


Brown, J. A., Sammy, M. J. in Ballinger, S. W. (2020). An evolutionary, or “Mitocentric” perspective on cellular function and disease. Redox Biology, 36, 101568. https://doi.org/https://doi.org/10.1016/j.redox.2020.101568



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