Abstract
Many diseases caused by mitochondrial dysfunction are caused by mitochondrial DNA abnormalities. The concept of mitochondrial therapy is based on the repair or removal of the existing anomaly. This can be done by replacing affected mitochondria by healthy ones, by in situ correction of the damaged mitochondrial DNA or by selective destruction of the affected mitochondria. In theory, all these concepts are applicable at the preconception stage, thus preventing the mother-to-child disease transmission, as well as at more advanced developmental stages (embryonic, fetal and postnatal) to alleviate disease symptoms in specific organs and tissues. Animal reasearch has paved the way to human therapies at all of these levels. So far, the only successful human application concerned the preconception stage and was based on replacement of diseased mitochondria in patients’ oocytes with healthy ones originating from oocytes donated by healthy women.
Highlights
Mitochondria are ubiquitous cell organelles that are responsible for generating energy needed for a variety of cell functions, but they are involved in multiple other cellular processes including calcium homeostasis, celular signaling and apoptosis [1]
A dual genetic control of mitochondrial function has been established, the optimal function resulting from a cooperation of proteins coded by mitochondrial own DNA and those coded by DNA of the hosting eukaryotic cell [1]
In addition to several tens of known mitochondrial diseases, related to mostly maternally inherited mutations in the human mitochondrial genome, it is suspected that de novo mutations in mitochondrial DNA are linked to other complex traits, including neurodegenerative diseases, aging and cancer [2]
Summary
Mitochondria are ubiquitous cell organelles that are responsible for generating energy needed for a variety of cell functions, but they are involved in multiple other cellular processes including calcium homeostasis, celular signaling and apoptosis [1]. New developments in molecular biology techniques, enabling a direct reparation of mitochondrial DNA mutations or selective destruction of the affected mitocondria, will hopefully make it possible to treat mitochondrial diseases at both preconception and postconception stages, without the need for recourse to third-party (donor) biological material.
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