en-28-643.pdf
www.ncbi.nlm.nih.gov/pmc/articles/PMC6946111/pdf/en-28-643.pdf
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hase; persistent SASP from senescent cells can lead to chronic inflammation and tissue dysfunction
g. mtDNA deletions are more frequent in the aging brain
g declines in ETC function, mitochondrial inner membrane function, and mitochondrial inte
During normal aging, the expression of some autophagy-associ- ated gen
, may decline in the human
ne
The minus-end-directed dynein and plus-end-directed
are key motor proteins that transport autophag
]. After tethering, autophagosome-ly
fusion is mediated by SNAR
. Autophagy plays an essential role in the clearance of damaged mitochond
[48]. In mETC deficient cells, O2•− production is blocked under starvation conditions, thereby reducing the activation of AMPK and increas- ing activation of the mTOR pathway, which results in a reduction of starvation-induced autoph
ion. A declining a
ab
repair DNA and consequent accumulation of DNA dama
contribute to cellular senesce
ve implicated defective DNA repair system in
ar, accumulation of p62 has been o
after loss of autophagy, which interrupts DNA damage re
tion, supp
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