In neurological disease and diabetes, the unfolded protein response (UPR) has been investigated for years, while its function in heart disease is less well understood. All three branches of the UPR are involved in ischaemia/reperfusion and can either protect or impair heart function. Recently, UPR has been found to play a role in arrhythmogenesis during human heart failure, and blocking UPR has an antiarrhythmic effect. This review will discuss the rationale for and challenges to targeting UPR in heart disease.
Keywords: activating transcription factor 6α; glucose-regulated protein-78; heart failure; inositol-requiring ER-to-nucleus signal kinase 1; ischaemia; protein kinase-like ER kinase.