Research Progress and Prospects in Mitochondrial DNA Repair and Exercise Stress
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Graphical Abstract
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Abstract
Due to the specific function of mitochondrion, mitochondrial DNA(mtDNA) is more fragile than nuclear DNA(nDNA).If the mtDNA damage can't be repaired, the accumulated damage will induce mitochondrial dysfunction. Therefore, mtDNA repair is an essential step in the quality control of mitochondrion. Based on the latest research on mtDNA repair, the mitochondrial DNA polymerase γ(POLG), nicotinamide adenine dinucleotide(NAD+/NADH)-NAD+dependent histone deacetylase(SIRT), 8-oxoguanine DNA glycosylase(OGG1) and P53 are suggested as key molecules in mediating mtDNA repair in this study. In addition,exercise can promote mtDNA repair by regulating the classic base excision repair(BER) pathway through Sirt3-OGG1 and P53.This study also explored the possible mechanism of exercise stress on mtDNA repair and the pathway of mtDNA repair related molecules to mediate exercise adaptation, which is expected to provide new theoretical thoughts for further research.
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