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AMP-activated protein kinase (AMPK) controls the aging process via an integrated signaling network
Author(s):
Antero Salminen
,
Kai Kaarniranta
Publication date
Created:
April 2012
Publication date
(Print):
April 2012
Journal:
Ageing Research Reviews
Publisher:
Elsevier BV
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Abstract
Efficient control of energy metabolic homeostasis, enhanced stress resistance, and qualified cellular housekeeping are the hallmarks of improved healthspan and extended lifespan. AMPK signaling is involved in the regulation of all these characteristics via an integrated signaling network. Many studies with lower organisms have revealed that increased AMPK activity can extend the lifespan. Experiments in mammals have demonstrated that AMPK controls autophagy through mTOR and ULK1 signaling which augment the quality of cellular housekeeping. Moreover, AMPK-induced stimulation of FoxO/DAF-16, Nrf2/SKN-1, and SIRT1 signaling pathways improves cellular stress resistance. Furthermore, inhibition of NF-κB signaling by AMPK suppresses inflammatory responses. Emerging studies indicate that the responsiveness of AMPK signaling clearly declines with aging. The loss of sensitivity of AMPK activation to cellular stress impairs metabolic regulation, increases oxidative stress and reduces autophagic clearance. These age-related changes activate innate immunity defence, triggering a low-grade inflammation and metabolic disorders. We will review in detail the signaling pathways of this integrated network through which AMPK controls energy metabolism, autophagic degradation and stress resistance and ultimately the aging process. Copyright © 2011 Elsevier B.V. All rights reserved.
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Neuronal Signaling
Author and article information
Journal
Title:
Ageing Research Reviews
Abbreviated Title:
Ageing Research Reviews
Publisher:
Elsevier BV
ISSN (Print):
15681637
Publication date Created:
April 2012
Publication date (Print):
April 2012
Volume
: 11
Issue
: 2
Pages
: 230-241
Article
DOI:
10.1016/j.arr.2011.12.005
PubMed ID:
22186033
SO-VID:
89f24257-b85b-4013-baab-0fd69514f70b
Copyright ©
© 2012
License:
https://www.elsevier.com/tdm/userlicense/1.0/
http://creativecommons.org/licenses/by-nc-nd/3.0/
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