PMID- 24370004
OWN - NLM
STAT- MEDLINE
DCOM- 20141029
LR  - 20211203
IS  - 1879-3061 (Electronic)
IS  - 1043-2760 (Print)
IS  - 1043-2760 (Linking)
VI  - 25
IP  - 3
DP  - 2014 Mar
TI  - Cardiomyocyte health: adapting to metabolic changes through autophagy.
PG  - 156-64
LID - S1043-2760(13)00205-1 [pii]
LID - 10.1016/j.tem.2013.11.004 [doi]
AB  - Autophagy is important in the heart for maintaining homeostasis when changes in 
      nutrient levels occur. Autophagy is involved in the turnover of cellular 
      components, and is rapidly upregulated during stress. Studies have found that 
      autophagy is reduced in metabolic disorders including obesity and diabetes. This 
      leads to accumulation of protein aggregates and dysfunctional organelles, which 
      contributes to the pathogenesis of cardiovascular disease. Autophagy is primarily 
      regulated by two components: the mechanistic target of rapamycin (mTOR) and 
      AMP-activated protein kinase (AMPK). Although mTOR integrates information about 
      growth factors and nutrients and is a negative regulator of autophagy, AMPK is an 
      energy sensor and activates autophagy when energy levels are low. These pathways 
      therefore present targets for the development of autophagy-modulating therapies.
CI  - Copyright (c) 2013 Elsevier Ltd. All rights reserved.
FAU - Kubli, Dieter A
AU  - Kubli DA
AD  - Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California 
      San Diego, La Jolla, CA 92093, USA.
FAU - Gustafsson, Asa B
AU  - Gustafsson AB
AD  - Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California 
      San Diego, La Jolla, CA 92093, USA. Electronic address: asag@ucsd.edu.
LA  - eng
GR  - R01 HL087023/HL/NHLBI NIH HHS/United States
GR  - P01HL085577/HL/NHLBI NIH HHS/United States
GR  - R01HL101217/HL/NHLBI NIH HHS/United States
GR  - R01HL092136/HL/NHLBI NIH HHS/United States
GR  - R01 HL101217/HL/NHLBI NIH HHS/United States
GR  - R01 HL092136/HL/NHLBI NIH HHS/United States
GR  - P01 HL085577/HL/NHLBI NIH HHS/United States
GR  - R01HL087023/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
DEP - 20131224
PL  - United States
TA  - Trends Endocrinol Metab
JT  - Trends in endocrinology and metabolism: TEM
JID - 9001516
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
SB  - IM
MH  - AMP-Activated Protein Kinases/metabolism
MH  - Animals
MH  - Autophagy/*physiology
MH  - Humans
MH  - Myocytes, Cardiac/*metabolism
MH  - TOR Serine-Threonine Kinases/metabolism
PMC - PMC3951169
MID - NIHMS552342
OTO - NOTNLM
OT  - AMPK
OT  - autophagy
OT  - diabetes
OT  - heart
OT  - mTOR
OT  - obesity
EDAT- 2013/12/29 06:00
MHDA- 2014/10/30 06:00
PMCR- 2015/03/01
CRDT- 2013/12/28 06:00
PHST- 2013/09/18 00:00 [received]
PHST- 2013/11/12 00:00 [revised]
PHST- 2013/11/22 00:00 [accepted]
PHST- 2013/12/28 06:00 [entrez]
PHST- 2013/12/29 06:00 [pubmed]
PHST- 2014/10/30 06:00 [medline]
PHST- 2015/03/01 00:00 [pmc-release]
AID - S1043-2760(13)00205-1 [pii]
AID - 10.1016/j.tem.2013.11.004 [doi]
PST - ppublish
SO  - Trends Endocrinol Metab. 2014 Mar;25(3):156-64. doi: 10.1016/j.tem.2013.11.004. 
      Epub 2013 Dec 24.