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Mitochondria, metabolism and aging
Author(s) -
Finkel Toren
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.342.1
Subject(s) - mitophagy , calorie restriction , autophagy , longevity , pi3k/akt/mtor pathway , mitochondrion , microbiology and biotechnology , mediator , biology , flux (metallurgy) , genetics , signal transduction , chemistry , apoptosis , endocrinology , organic chemistry
The molecular pathways controlling lifespan are incompletely understood. One strategy to increase the longevity of multiple diverse organisms is through caloric restriction. Evidence suggests that the mTOR pathway might be an important mediator of the effect of calorie restriction. Here, I will describe two mouse models that my lab has generated. The first is a mouse model of reduced mTOR expression that results in an increase in overall lifespan as well as a segmental increase in healthspan. The molecular basis of these effects, i.e. how a reduction in mTOR signaling promotes longevity is not known. One potential pathway, however, is through augmenting autophaic flux. For the second part of my talk, I will describe a second mouse model that allows for a more accurate assessment of in vivo mitophagy, namely the selective removal of damaged mitochondria. This mouse allowed us to quantify how mitophagy changes as a function of age. These results suggest that a decline in autophagic flux might fuel the aging process. Support or Funding Information This work was supported by NHLBI Intramural and extramural funds This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .