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Protofection is the transfection of foreign mitochondrial DNA into the mitochondria of all cells in a tissue to supplement or replace the native mitochondrial DNA already present. As mitochondrial DNA becomes progressively more damaged with age, this may provide a method of at least partially rejuvenating mitochondria in old tissue, restoring them to their original, youthful function. It is thought that mitochondrial damage and dysfunction play an important role in aging: see the mitochondrial free radical theory of aging. Protofection is also a basis for constructing gene therapies for inherited genetic diseases such as Leber's hereditary optic neuropathy in which mitochondrial DNA is mutated. This technology could similarly be applied to modified or artificial mitochondria. The intent being designing ones that do not produce as many (preferably zero) free radicals while staying as, or more efficient in generating energy in the cell. While not invulnerable to free radical damage, having less free radicals would also make such generators have longer lifespans if they could still renew at an identical rate, or at least enough to keep more healthy ones at a given time. ==External links== *(What Happened to Protofection? ) An article giving some context for the past few years of protofection development. *(Mitochondrial Gene Therapy Augments Mitochondrial Physiology in a Parkinson's Disease Cell Model ) *(Development of Mitochondrial Gene Replacement Therapy ) *(Novel Therapeutic Approaches for Leber's Hereditary Optic Neuropathy ) 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「Protofection」の詳細全文を読む スポンサード リンク
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