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Autophagy accounts for approximately one-third of mitochondrial protein turnover and is protein selective.

The remarkable comment in the abstract to me was the following: "We found that ~35% of mitochondrial protein turnover occurred via autophagy. Similar analyses using parkin mutants revealed that parkin-dependent mitophagy accounted for ~25% of mitochondrial protein turnover, suggesting that most mitochondrial autophagy specifically eliminates dysfunctional mitochondria." This last seems particularly important. Could this selective elimination of dysfunctional mitochondria include clonally expanded mutants? If so, is there some way to enhance this process?
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Age Dependent Dysfunction of Mitochondrial and ROS Metabolism Induced by Mitonuclear Mismatch.

I thought I heard some discussion among SENS researchers about tRNAs in the context of MitoSENS. I won't pretend to understand the exact details of "mitonuclear mismatch" of tRNA sequences and how they might arise during human aging (I suspect it may be simply from mtDNA mutations, if this mismatch happens at all), but I thought some mitochondrial researchers may want to look at this report.
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Increased dNTP pools rescue mtDNA depletion in human POLG-deficient fibroblasts.

Because this work was done in a model of POLG-deficiency, it's not clear to me that this has any relevance to age-related mtDNA problems. But the intervention and results were interesting and relevant to mtDNA maintenance, so I'm including it in case it is relevant. This group reported that increasing the concentration of deoxynucleotide triphosphates to mitochondria could restore mtDNA depletion in this model. They suggest this might be relevant for "other conditions in which mtDNA maintenance is challenged"; couldn't aging be characterized in this way? But perhaps aging is not characterized by POLG deficiency, so this particular intervention may not be useful.
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Free report on high blood pressure

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Free diabetes report

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