Autophagy modulation: A potential therapeutic approach in cardiac hypertrophy

Xuejun Wang, Taixing Cui

Research output: Contribution to journalReview article

22 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)H304-H319
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume313
Issue number2
DOIs
StatePublished - Aug 11 2017

Fingerprint

Autophagy
Cardiomegaly
Heart Failure
Lysosomes
Pressure
Therapeutics
Recycling
Quality Control
Autophagosomes

Keywords

  • Autophagy
  • Cardiac hypertrophy
  • Mechanistic target of rapamycin
  • Pressure overload
  • Transcription factor EB

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Autophagy modulation : A potential therapeutic approach in cardiac hypertrophy. / Wang, Xuejun; Cui, Taixing.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 313, No. 2, 11.08.2017, p. H304-H319.

Research output: Contribution to journalReview article

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