Abstract
Transplantation of functional mitochondria directly into defective cells is a novel approach that has recently caught the attention of scientists and the general public alike. Could this be too good to be true?
Highlights
Mitochondrial transfer is a potential cure for many diseases but proof of efficacy and safety is still lacking Robert N Lightowlers1,*, Zofia MA Chrzanowska-Lightowlers1 & Oliver M Russell2
Treatment strategies for mitochondrial dysfunction in general fall into the following categories: (i) increasing mitochondrial biogenesis; (ii) reducing dysfunctional mitochondria and replacing them with active ones; (iii) by-passing or substituting the defective component; (iv) targeting the consequences of mitochondrial dysfunction; or (v) reprogramming metabolism (Russell et al, 2020)
One concept that was not addressed in the above-mentioned review (Russell et al, 2020) is whether increasing mitochondrial bulk by mitochondrial transplantation per se could be a viable approach—which we address in this article
Summary
While many mitochondrial diseases affect neurological function, defective mitochondria can affect any tissue type and symptoms are often multisystemic and complex. The mitochondrion contains its own genome, mtDNA, that encodes just thirteen of the more than 1,000 polypeptides that comprise the mitochondrion. Pathogenic mutations that cause mitochondrial disease can occur in either genome. Adults tend to have mutations in mtDNA, whereas severe neonatal defects have aberrant nuclear genes. Mitochondrial disease is amongst the most common form of inherited neurological disorder with a minimum prevalence of 1:5,000
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