PMID- 25771142
OWN - NLM
STAT- MEDLINE
DCOM- 20160407
LR  - 20200929
IS  - 1095-8584 (Electronic)
IS  - 0022-2828 (Linking)
VI  - 84
DP  - 2015 Jul
TI  - Too much or not enough of a good thing--The Janus faces of autophagy in cardiac 
      fuel and protein homeostasis.
PG  - 223-6
LID - S0022-2828(15)00075-9 [pii]
LID - 10.1016/j.yjmcc.2015.03.001 [doi]
AB  - Cells respond to changes in their environment and in their intracellular milieu 
      by altering specific pathways of protein synthesis and degradation. Autophagy is 
      a highly conserved catabolic process involved in the degradation of long-lived 
      proteins, damaged organelles, and subcellular structures. The process is 
      orchestrated by the autophagy related protein (Atg) to form the double-membrane 
      structure autophagosomes, which then fuse with lysosomes to generate 
      autophagolysosomes where subcellular contents are degraded for a variety of 
      cellular processes. Alterations in autophagy play an important role in diseases 
      including cancer, neurodegenerative diseases, aging, metabolic diseases, 
      inflammation and cardiovascular diseases. In the latter, dysregulated autophagy 
      is speculated to contribute to the onset and development of atherosclerosis, 
      ischemia/reperfusion injury, cardiomyopathy, diabetes mellitus, and hypertension. 
      Autophagy may be both adaptive and beneficial for cell survival, or maladaptive 
      and detrimental for the cell. Basal autophagy plays an essential role in the 
      maintenance of cellular homeostasis whereas excessive autophagy may lead to 
      autophagic cell death. The point and counterpoint discussion highlights adaptive 
      vs. maladaptive autophagy. In this review, we discuss the molecular control of 
      autophagy, focusing particularly on the regulation of physiologic vs. defective 
      autophagy.
CI  - Copyright (c) 2015 Elsevier Ltd. All rights reserved.
FAU - Ren, Jun
AU  - Ren J
AD  - Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan 
      University, Shanghai 200032, China; Center for Cardiovascular Research and 
      Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, 
      WY, USA. Electronic address: jren@uwyo.edu.
FAU - Taegtmeyer, Heinrich
AU  - Taegtmeyer H
AD  - Department of Internal Medicine, Division of Cardiology, The University of Texas 
      Health Science Center, Houston, TX, USA. Electronic address: 
      Heinrich.Taegtmeyer@uth.tmc.edu.
LA  - eng
GR  - 5R01HL061483/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
DEP - 20150311
PL  - England
TA  - J Mol Cell Cardiol
JT  - Journal of molecular and cellular cardiology
JID - 0262322
RN  - 0 (Proteins)
SB  - IM
MH  - Animals
MH  - *Autophagy
MH  - *Homeostasis
MH  - Humans
MH  - Models, Biological
MH  - Myocardium/*cytology/*metabolism
MH  - Proteins/*metabolism
OTO - NOTNLM
OT  - Autophagy
OT  - Cell death
OT  - Heart diseases
OT  - Survival
EDAT- 2015/03/17 06:00
MHDA- 2016/04/08 06:00
CRDT- 2015/03/16 06:00
PHST- 2014/09/04 00:00 [received]
PHST- 2015/02/23 00:00 [revised]
PHST- 2015/03/02 00:00 [accepted]
PHST- 2015/03/16 06:00 [entrez]
PHST- 2015/03/17 06:00 [pubmed]
PHST- 2016/04/08 06:00 [medline]
AID - S0022-2828(15)00075-9 [pii]
AID - 10.1016/j.yjmcc.2015.03.001 [doi]
PST - ppublish
SO  - J Mol Cell Cardiol. 2015 Jul;84:223-6. doi: 10.1016/j.yjmcc.2015.03.001. Epub 
      2015 Mar 11.