Proteostasis and Beyond: ATF6 in Ischemic Disease

Christopher C. Glembotski, Jessica D. Rosarda, R. Luke Wiseman

Research output: Contribution to journalReview articlepeer-review

29 Scopus citations

Abstract

Endoplasmic reticulum (ER) stress is a pathological hallmark of numerous ischemic diseases, including stroke and myocardial infarction (MI). In these diseases, ER stress leads to activation of the unfolded protein response (UPR) and subsequent adaptation of cellular physiology in ways that dictate cellular fate following ischemia. Recent evidence highlights a protective role for the activating transcription factor 6 (ATF6) arm of the UPR in mitigating adverse outcomes associated with ischemia/reperfusion (I/R) injury in multiple disease models. This suggests ATF6 as a potential therapeutic target for intervening in diverse ischemia-related disorders. Here, we discuss the evidence demonstrating the importance of ATF6 signaling in protecting different tissues against ischemic damage and discuss preclinical results focused on defining the potential for pharmacologically targeting ATF6 to intervene in such diseases.

Original languageEnglish (US)
Pages (from-to)538-550
Number of pages13
JournalTrends in Molecular Medicine
Volume25
Issue number6
DOIs
StatePublished - Jun 2019
Externally publishedYes

Keywords

  • ATF6
  • ER stress
  • myocardial infarction
  • stroke
  • unfolded protein response

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology

Fingerprint

Dive into the research topics of 'Proteostasis and Beyond: ATF6 in Ischemic Disease'. Together they form a unique fingerprint.

Cite this