Ablation of C/EBP homologous protein attenuates endoplasmic reticulum-mediated apoptosis and cardiac dysfunction induced by pressure overload.

Background: Apoptosis may contribute to the development of heart failure, but the role of apoptotic signaling initiated by the endoplasmic reticulum in this condition has not been well clarified.

Methods And Results: In myocardial samples from patients with heart failure, quantitative real-time polymerase chain reaction revealed an increase in messenger RNA for C/EBP homologous protein (CHOP), a transcriptional factor that mediates endoplasmic reticulum-initiated apoptotic cell death. We performed transverse aortic constriction or sham operation on wild-type (WT) and CHOP-deficient mice.

X-box binding protein 1 regulates brain natriuretic peptide through a novel AP1/CRE-like element in cardiomyocytes.

The unfolded protein response (UPR) is triggered to assist protein folding when endoplasmic reticulum (ER) function is impaired. Recent studies demonstrated that ER stress can also induce cell-specific genes. In this study, we examined whether X-box binding protein 1 (XBP1), a major UPR-linked transcriptional factor, regulates the expression of brain natriuretic peptide (BNP) in cardiomyocytes.

Intravenous myocardial contrast echocardiography can predict recurrence of pressure gradient of left ventricular outflow tract in hypertrophic obstructive cardiomyopathy after percutaneous transluminal septal myocardial ablation.

Percutaneous transluminal septal myocardial ablation (PTSMA) is appropriate in patients who are refractory to medical treatments for hypertrophic obstructive cardiomyopathy (HOCM). However, about 10% of patients show recurrence of left ventricular outflow tract pressure gradient (LVOG) after PTSMA and need repeat PTSMA. The authors describe two HOCM cases who underwent intravenous myocardial contrast echocardiography (IVMCE) at two weeks after PTSMA.

Overexpression of endoplasmic reticulum-resident chaperone attenuates cardiomyocyte death induced by proteasome inhibition.

Aims: Proteasome inhibitors are a novel class of anticancer agents that induce tumour cell death via endoplasmic reticulum (ER) stress. Since ER stress is involved in the development of heart failure, we investigated the role of ER-initiated cardiomyocyte death by proteasome inhibition.

Methods And Results: Rat neonatal cardiomyocytes were used in this study.