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Keywords:

  • mitochondria;
  • mtDNA;
  • pharmacogenomics;
  • cybrid cell lines

Abstract

Preclinical Research

Several key components of the oxidative phosphorylation system are coded in mitochondrial DNA. In humans, the mutation rate of the mitochondrial genome is higher than that of nuclear DNA. Some of these mutations can modify the interaction of mitochondrial DNA-encoded products with different therapeutic drugs. Several of these mutations have survived evolution, therefore generating different mitochondrial DNA genetic backgrounds. Thus, personalized medicine approaches must consider these particular interactions. However, before incorporating this knowledge into patient treatments, cellular and molecular studies are required. In this review, we discuss the cybrid model as a tool for this type of analysis, along with the pitfalls and improvements that are necessary before the translation of such models to medical practice.