Calreticulin expression in human cardiac myocytes induces ER stress-associated apoptosis.

ABSTRACT: The global burden of heart failure following myocardial ischemia-reperfusion (IR) injury is a growing problem. One pathway that is key to understanding the progression of myocardial infarction and IR injury is the endoplasmic reticulum (ER) stress pathway, which contributes to apoptosis signaling and tissue death. The role of calreticulin in the progression of ER stress remains controversial. We hypothesized that calreticulin induction drives proapoptotic signaling in response to ER stress. We find here that calreticulin is upregulated in human ischemic heart failure cardiac tissue, as well as simulated hypoxia and reoxygenation (H/R) and thapsigargin-mediated ER stress. To test the impact of direct modulation of calreticulin expression on ER stress-induced apoptosis, human cardiac-derived

SUBMITTER: Stoner MW 

PROVIDER: S-EPMC7177173 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature