The endoplasmic reticulum (ER) serves several essential cellular functions including protein synthesis, protein folding, protein translocation, calcium homoeostasis and lipid biosynthesis. Physiological or pathological stimuli, which disrupt ER homoeostasis and disturb its functions, lead to an accumulation of misfolded and unfolded proteins, a condition referred to as ER stress. ER stress triggers the unfolded protein response to restore the homoeostasis of ER, through activating transcriptional and translational pathways. However, prolonged ER stress will lead to cell dysfunction and apoptosis. Recent evidence revealed that ER stress is involved in the development and progression of various heart diseases, such as cardiac hypertrophy, ischaemic heart diseases and heart failure. Therefore, improved understanding of the molecular mechanisms of ER stress in heart disease will help to investigate more potential targets for new therapeutic interventions and drug discovery.
Linked articles: This article is part of a themed section on Spotlight on Small Molecules in Cardiovascular Diseases. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.8/issuetoc.
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