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@ARTICLE{Ehninger:137629,
author = {Ehninger, Dan and Neff, Frauke and Xie, Kan},
title = {{L}ongevity, aging and rapamycin.},
journal = {Cellular and molecular life sciences},
volume = {71},
number = {22},
issn = {1420-682X},
address = {Cham (ZG)},
publisher = {Springer International Publishing AG},
reportid = {DZNE-2020-03951},
pages = {4325-4346},
year = {2014},
abstract = {The federal drug administration (FDA)-approved compound
rapamycin was the first pharmacological agent shown to
extend maximal lifespan in both genders in a mammalian
species. A major question then is whether the drug slows
mammalian aging or if it has isolated effects on longevity
by suppressing cancers, the main cause of death in many
mouse strains. Here, we review what is currently known about
the effects that pharmacological or genetic mammalian target
of rapamycin (mTOR) inhibition have on mammalian aging and
longevity. Currently available evidence seems to best fit a
model, wherein rapamycin extends lifespan by suppressing
cancers. In addition the drug has symptomatic effects on
some aging traits, such as age-related cognitive
impairments.},
subtyp = {Review Article},
keywords = {Aging / Animals / Antibiotics, Antineoplastic: pharmacology
/ Gene Expression Regulation: drug effects / Humans /
Longevity: drug effects / Neurons: drug effects / Neurons:
metabolism / Signal Transduction: drug effects / Sirolimus:
pharmacology / TOR Serine-Threonine Kinases: metabolism /
Antibiotics, Antineoplastic (NLM Chemicals) / TOR
Serine-Threonine Kinases (NLM Chemicals) / Sirolimus (NLM
Chemicals)},
cin = {AG Ehninger},
ddc = {610},
cid = {I:(DE-2719)1013005},
pnm = {342 - Disease Mechanisms and Model Systems (POF3-342)},
pid = {G:(DE-HGF)POF3-342},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:25015322},
pmc = {pmc:PMC4207939},
doi = {10.1007/s00018-014-1677-1},
url = {https://pub.dzne.de/record/137629},
}