Autophagy modulation: a potential therapeutic approach in cardiac hypertrophy

Autophagy is an evolutionarily conserved process used by the cell to degrade cytoplasmic contents for quality control, survival for temporal energy crisis, and catabolism and recycling. Rapidly increasing evidence has revealed an important pathogenic role of altered activity of the autophagosome-lys...

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Published inAmerican journal of physiology. Heart and circulatory physiology Vol. 313; no. 2; pp. H304 - H319
Main Authors Wang, Xuejun, Cui, Taixing
Format Journal Article
LanguageEnglish
Published United States American Physiological Society 01.08.2017
SeriesHeart Failure: Novel Therapeutic Pathways Emerging from Basic Science
Subjects
Animals
Autophagy
Blood pressure
Cardiomegaly - metabolism
Cardiomegaly - pathology
Cardiomegaly - physiopathology
Cardiomegaly - therapy
Cardiovascular system
Catabolism
Cytoplasm
Heart failure
Heart Failure - metabolism
Heart Failure - pathology
Heart Failure - physiopathology
Heart Failure - therapy
Humans
Lysosomes - metabolism
Lysosomes - pathology
Myocardium - metabolism
Myocardium - pathology
Quality control
Review
Signal Transduction
transcription factor EB
autophagy
mechanistic target of rapamycin
cardiac hypertrophy
pressure overload
Online AccessGet full text
ISSN0363-6135
1522-1539
1522-1539
DOI10.1152/ajpheart.00145.2017

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Abstract Autophagy is an evolutionarily conserved process used by the cell to degrade cytoplasmic contents for quality control, survival for temporal energy crisis, and catabolism and recycling. Rapidly increasing evidence has revealed an important pathogenic role of altered activity of the autophagosome-lysosome pathway (ALP) in cardiac hypertrophy and heart failure. Although an early study suggested that cardiac autophagy is increased and that this increase is maladaptive to the heart subject to pressure overload, more recent reports have overwhelmingly supported that myocardial ALP insufficiency results from chronic pressure overload and contributes to maladaptive cardiac remodeling and heart failure. This review examines multiple lines of preclinical evidence derived from recent studies regarding the role of autophagic dysfunction in pressure-overloaded hearts, attempts to reconcile the discrepancies, and proposes that resuming or improving ALP flux through coordinated enhancement of both the formation and the removal of autophagosomes would benefit the treatment of cardiac hypertrophy and heart failure resulting from chronic pressure overload.
AbstractList Autophagy is an evolutionarily conserved process used by the cell to degrade cytoplasmic contents for quality control, survival for temporal energy crisis, and catabolism and recycling. Rapidly increasing evidence has revealed an important pathogenic role of altered activity of the autophagosome-lysosome pathway (ALP) in cardiac hypertrophy and heart failure. Although an early study suggested that cardiac autophagy is increased and that this increase is maladaptive to the heart subject to pressure overload, more recent reports have overwhelmingly supported that myocardial ALP insufficiency results from chronic pressure overload and contributes to maladaptive cardiac remodeling and heart failure. This review examines multiple lines of preclinical evidence derived from recent studies regarding the role of autophagic dysfunction in pressure-overloaded hearts, attempts to reconcile the discrepancies, and proposes that resuming or improving ALP flux through coordinated enhancement of both the formation and the removal of autophagosomes would benefit the treatment of cardiac hypertrophy and heart failure resulting from chronic pressure overload.
Autophagy is an evolutionarily conserved process used by the cell to degrade cytoplasmic contents for quality control, survival for temporal energy crisis, and catabolism and recycling. Rapidly increasing evidence has revealed an important pathogenic role of altered activity of the autophagosome-lysosome pathway (ALP) in cardiac hypertrophy and heart failure. Although an early study suggested that cardiac autophagy is increased and that this increase is maladaptive to the heart subject to pressure overload, more recent reports have overwhelmingly supported that myocardial ALP insufficiency results from chronic pressure overload and contributes to maladaptive cardiac remodeling and heart failure. This review examines multiple lines of preclinical evidence derived from recent studies regarding the role of autophagic dysfunction in pressure-overloaded hearts, attempts to reconcile the discrepancies, and proposes that resuming or improving ALP flux through coordinated enhancement of both the formation and the removal of autophagosomes would benefit the treatment of cardiac hypertrophy and heart failure resulting from chronic pressure overload.Autophagy is an evolutionarily conserved process used by the cell to degrade cytoplasmic contents for quality control, survival for temporal energy crisis, and catabolism and recycling. Rapidly increasing evidence has revealed an important pathogenic role of altered activity of the autophagosome-lysosome pathway (ALP) in cardiac hypertrophy and heart failure. Although an early study suggested that cardiac autophagy is increased and that this increase is maladaptive to the heart subject to pressure overload, more recent reports have overwhelmingly supported that myocardial ALP insufficiency results from chronic pressure overload and contributes to maladaptive cardiac remodeling and heart failure. This review examines multiple lines of preclinical evidence derived from recent studies regarding the role of autophagic dysfunction in pressure-overloaded hearts, attempts to reconcile the discrepancies, and proposes that resuming or improving ALP flux through coordinated enhancement of both the formation and the removal of autophagosomes would benefit the treatment of cardiac hypertrophy and heart failure resulting from chronic pressure overload.
Author Wang, Xuejun
Cui, Taixing
Author_xml – sequence: 1
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  surname: Cui
  fullname: Cui, Taixing
  organization: Department of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina
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Keywords transcription factor EB
autophagy
mechanistic target of rapamycin
cardiac hypertrophy
pressure overload
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Snippet Autophagy is an evolutionarily conserved process used by the cell to degrade cytoplasmic contents for quality control, survival for temporal energy crisis, and...
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SubjectTerms Animals
Autophagy
Blood pressure
Cardiomegaly - metabolism
Cardiomegaly - pathology
Cardiomegaly - physiopathology
Cardiomegaly - therapy
Cardiovascular system
Catabolism
Cytoplasm
Heart failure
Heart Failure - metabolism
Heart Failure - pathology
Heart Failure - physiopathology
Heart Failure - therapy
Humans
Lysosomes - metabolism
Lysosomes - pathology
Myocardium - metabolism
Myocardium - pathology
Quality control
Review
Signal Transduction
Title Autophagy modulation: a potential therapeutic approach in cardiac hypertrophy
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https://pubmed.ncbi.nlm.nih.gov/PMC5582915
Volume 313
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