Document Detail


Pharmacological modulation of autophagy during cardiac stress.
MedLine Citation:
PMID:  22710813     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Autophagy is an evolutionarily conserved intracellular mechanism for degradation of long-lived proteins and organelles. Accumulating lines of evidence indicate that autophagy is deeply involved in the development of cardiac disease. Autophagy is upregulated in almost all cardiac pathological states, exerting both protective and detrimental functions. Whether autophagy activation is an adaptive or maladaptive mechanism during cardiac stress seems to depend upon the pathological context in which it is upregulated, the extent of its activation, and the signaling mechanisms promoting its enhancement. Pharmacological modulation of autophagy may therefore represent a potential therapeutic strategy to limit myocardial damage during cardiac stress. Several pharmacological agents that are able to modulate autophagy have been identified, such as mammalian target of rapamycin inhibitors, adenosine monophosphate-dependent kinase modulators, sirtuin activators, myo-inositol-1,4,5-triphosphate and calcium-lowering agents, and lysosome inhibitors. Although few of these modulators of autophagy have been directly tested during cardiac stress, many of them seem to have high potential to be efficient in the treatment of cardiac disease. We will discuss the potential usefulness of different pharmacological activators and inhibitors of autophagy in the treatment of cardiac diseases.
Authors:
Sebastiano Sciarretta; Peiyong Zhai; Massimo Volpe; Junichi Sadoshima
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Journal of cardiovascular pharmacology     Volume:  60     ISSN:  1533-4023     ISO Abbreviation:  J. Cardiovasc. Pharmacol.     Publication Date:  2012 Sep 
Date Detail:
Created Date:  2012-09-11     Completed Date:  2013-07-09     Revised Date:  2013-09-03    
Medline Journal Info:
Nlm Unique ID:  7902492     Medline TA:  J Cardiovasc Pharmacol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  235-41     Citation Subset:  IM    
Affiliation:
Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark, NJ 07103, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Autophagy / drug effects*,  physiology
Cardiovascular Agents / pharmacology,  therapeutic use*
Enzyme Inhibitors / pharmacology,  therapeutic use
Heart Diseases / drug therapy*,  metabolism,  pathology
Humans
Inositol 1,4,5-Trisphosphate / antagonists & inhibitors,  metabolism
Stress, Physiological / drug effects*,  physiology
TOR Serine-Threonine Kinases / antagonists & inhibitors*,  metabolism
Grant Support
ID/Acronym/Agency:
AG23039/AG/NIA NIH HHS; AG27211/AG/NIA NIH HHS; HL102738/HL/NHLBI NIH HHS; HL67724/HL/NHLBI NIH HHS; HL69020/HL/NHLBI NIH HHS; HL91469/HL/NHLBI NIH HHS; R01 AG023039/AG/NIA NIH HHS; R01 AG028787/AG/NIA NIH HHS; R01 HL067724/HL/NHLBI NIH HHS; R01 HL067727/HL/NHLBI NIH HHS; R01 HL091469/HL/NHLBI NIH HHS; R01 HL102738/HL/NHLBI NIH HHS; R01 HL112330/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Cardiovascular Agents; 0/Enzyme Inhibitors; 85166-31-0/Inositol 1,4,5-Trisphosphate; EC 2.7.1.1/MTOR protein, human; EC 2.7.1.1/TOR Serine-Threonine Kinases
Comments/Corrections

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