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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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Autophagy Is Required for Memory Formation and Reverses Age-Related Memory Decline.

I thought I've seen some reports of autophagy being downregulated or less active during aging, at least in some tissues. This group reports that age-related decline of autophagy in the hippocampus may be a cause of age-related memory impairment, and in mice, "restoration" of autophagy with young plasma "rejuvenates memory in an autophagy-dependent manner". They also report that osteocalcin appears to be "a direct hormonal inducer of hippocampal autophagy", which they identified in young plasma.
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Insulin in high concentration recede cigarette smoke extract induced cellular senescence of airway epithelial cell through autophagy pathway.

The authors seem to be using the word "recede" subtly incorrectly. If I'm understanding them correctly, this report seems to say that treatment of some types of lung cells with insulin or rapamycin would "recede" (reverse?) senescence markers and enhance autophagy. I would expect this from rapamycin, but that insulin apparently accomplished this seems particularly interesting; it reminds me of some reports of using intranasal insulin in the treatment of Alzheimer's or other neurodegenerative disorders.
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MicroRNA-29 enhances autophagy and cleanses exogenous mutant αB-crystallin in retinal pigment epithelial cells.

From this report, it appears that miR-29 may have an important role in regulating autophagy, at least in RPE cells in cell culture. This group reported that miR-29 overexpression increased autophagic activity, but from the abstract, they apparently didn't observe a reduction in lipofuscin or drusen--something they said they tried to find. But they did note that miR-29 overexpression "enhances autophagy which aids in the removal of protein aggregates".
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Therapeutic activation of autophagy by combined treatment with rapamycin and trehalose in a mouse MPTP-induced model of Parkinson’s disease.

I have reported previously on the ability of trehalose to induce autophagy, though some reports suggest that *oral* trelhalose does *not* do so. This group reports that a combination of rapamycin and oral trehalose additively enhanced autophagy in a mouse model of Parkinson's disease, with some significant, positive effects observed from this combined treatment.
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Autophagy in Human Skin Fibroblasts: Impact of Age.

I suspect this report is interesting to this group because I sometimes read that either mTOR is upregulated in aging, autophagy is downregulated, or both. This group reports that neither appears to be the case in human skin fibroblasts, which appear to have similar levels of mTOR, autophagy proteins, and the number of autophagosomes per cytoplasmic area. The researchers suggest that for whatever reason, there may be more material needing degraded in aging tissue, such that normal autophagic function is not sufficient to process it and keep cells functioning well.
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TFEB-dependent induction of thermogenesis by the hepatocyte SLC2A inhibitor trehalose.

I suspect I might be mistakenly reporting this paper out of personal interest, rather than the paper's relevance to rejuvenation biotech. With its relation to TFEB and autohpagy, I decided to err on the side of reporting it. Interestingly, this group reports a connection between autophagy, uncoupling, and thermogenesis. They found that *oral* administration of trehalose in mice: (1) induced hepatocyte TFEB, (2) increased expression of UCP1 in hepatocytes and white adipocytes, and (3) increased light- and day-cycle thermogenesis. Moreover, they found that hepatocyte-selective TFEB knockdown abolished trehalose induction of thermogenesis and WAT UCP1, suggesting that liver autophagy may have something to do with WAT uncoupling. Finally, they report that the increased thermogenesis was independent of leptin. They suggest that these effects might be relevant to treating obesity and type 2 diabetes, but I doubt the effect will be strong enough to offset self-destructive eating habits if they are too severe.
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