The role of the unfolded protein response in the heart

Research output: Contribution to journalReview articlepeer-review

103 Scopus citations

Abstract

The misfolding of nascent proteins, or the unfolding of proteins after synthesis is complete, can occur in response to numerous environmental stresses, or as a result of mutations that de-stabilize protein structure. Cells have developed elaborate protein quality control systems that recognize improperly folded proteins and either refold them or facilitate their degradation. One such quality control system is the unfolded protein response, or the UPR. The UPR is a highly conserved signal transduction system that is activated when cells are subjected to conditions that alter the endoplasmic reticulum (ER) in ways that impair the folding of nascent proteins in this organelle. Recent observations indicate that in the heart, the UPR is activated during acute stresses, including ischemia/reperfusion, as well as upon longer term stresses that lead to cardiac hypertrophy and heart failure. Moreover, certain aspects of the UPR are activated during, and are required for proper heart development. This review summarizes recent studies of the UPR in the heart, focusing on the possible roles of the UPR in contributing to, or protecting from ischemia/reperfusion damage.

Original languageEnglish (US)
Pages (from-to)453-459
Number of pages7
JournalJournal of Molecular and Cellular Cardiology
Volume44
Issue number3
DOIs
StatePublished - Mar 2008
Externally publishedYes

Keywords

  • ER stress
  • Ischemia
  • Ischemia/Reperfusion
  • Unfolded protein response

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine

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