PMID- 31572724
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 2296-634X (Print)
IS  - 2296-634X (Electronic)
IS  - 2296-634X (Linking)
VI  - 7
DP  - 2019
TI  - Pleiotropic Effects of mTOR and Autophagy During Development and Aging.
PG  - 192
LID - 10.3389/fcell.2019.00192 [doi]
LID - 192
AB  - Autophagy as a ubiquitous catabolic process causes degradation of cytoplasmic 
      components and is generally considered to have beneficial effects on health and 
      lifespan. In contrast, inefficient autophagy has been linked with detrimental 
      effects on the organism and various diseases, such as Parkinson's disease. 
      Previous research, however, showed that this paradigm is far from being black and 
      white. For instance, it has been reported that increased levels of autophagy 
      during development can be harmful, but become advantageous in the aging cell or 
      organism, causing enhanced healthspan and even longevity. The antagonistic 
      pleiotropy hypothesis postulates that genes, which control various traits in an 
      organism, can be fitness-promoting in early life, but subsequently trigger aging 
      processes later. Autophagy is controlled by the mechanistic target of rapamycin 
      (mTOR), a key player of nutrient sensing and signaling and classic example of a 
      pleiotropic gene. mTOR acts upstream of transcription factors such as FOXO, NRF, 
      and TFEB, controlling protein synthesis, degradation, and cellular growth, 
      thereby regulating fertility as well as aging. Here, we review recent findings 
      about the pleiotropic role of autophagy during development and aging, examine the 
      upstream factors, and contemplate specific mechanisms leading to disease, 
      especially neurodegeneration.
CI  - Copyright (c) 2019 Schmeisser and Parker.
FAU - Schmeisser, Kathrin
AU  - Schmeisser K
AD  - Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.
FAU - Parker, J Alex
AU  - Parker JA
AD  - Departement de Neurosciences, Universite de Montreal, Montreal, QC, Canada.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20190911
PL  - Switzerland
TA  - Front Cell Dev Biol
JT  - Frontiers in cell and developmental biology
JID - 101630250
PMC - PMC6749033
OTO - NOTNLM
OT  - C. elegans
OT  - aging
OT  - autophagy
OT  - genetics
OT  - pleiotropy
EDAT- 2019/10/02 06:00
MHDA- 2019/10/02 06:01
PMCR- 2019/01/01
CRDT- 2019/10/02 06:00
PHST- 2019/04/30 00:00 [received]
PHST- 2019/08/27 00:00 [accepted]
PHST- 2019/10/02 06:00 [entrez]
PHST- 2019/10/02 06:00 [pubmed]
PHST- 2019/10/02 06:01 [medline]
PHST- 2019/01/01 00:00 [pmc-release]
AID - 10.3389/fcell.2019.00192 [doi]
PST - epublish
SO  - Front Cell Dev Biol. 2019 Sep 11;7:192. doi: 10.3389/fcell.2019.00192. 
      eCollection 2019.