Autophagy and proteotoxicity in cardiomyocytes

J. Scott Pattison, Jeffrey Robbins

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Increasing evidence suggests that misfolded proteins and intracellular aggregates contribute to cardiac disease and heart failure. We wished to determine if autophagic induction by Atg7 is sufficient to reduce misfolded protein and aggregate content in protein misfolding-stressed cardiomyocytes. We used loss- and gain-of-function approaches in cultured cardiomyocytes to determine the effects of ATG7 knockdown and Atg7 overexpression in protein conformation-based toxicity induced by expression of a mutant aB crystallin (CryABR120G) known to cause human heart disease. We show that Atg7 induces basal autophagy and rescues the CryAB accumulation of misfolded proteins and aggregates in cardiomyocytes.

Original languageEnglish (US)
Pages (from-to)1259-1260
Number of pages2
JournalAutophagy
Volume7
Issue number10
DOIs
StatePublished - Oct 2011

Fingerprint

Autophagy
Cardiac Myocytes
Heart Diseases
Heart Failure
Protein Conformation
Crystallins
Protein Aggregates
Proteins

Keywords

  • Autophagy
  • Cardiomyopathy
  • Cell death
  • Heart
  • Protein misfolding

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

Cite this

Autophagy and proteotoxicity in cardiomyocytes. / Pattison, J. Scott; Robbins, Jeffrey.

In: Autophagy, Vol. 7, No. 10, 10.2011, p. 1259-1260.

Research output: Contribution to journalArticle

Pattison, J. Scott ; Robbins, Jeffrey. / Autophagy and proteotoxicity in cardiomyocytes. In: Autophagy. 2011 ; Vol. 7, No. 10. pp. 1259-1260.
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