Endoplasmic reticulum stress in the pathogenesis of hypertension

Abstract

The endoplasmic reticulum (ER) is a cellular organelle specialized in the synthesis, folding, assembly, and modification of proteins. In situations of increased protein demand, complex signaling pathways, termed the unfolded protein response (UPR), influence a series of cellular feedback loops to strictly control ER function. While initially a compensatory attempt to maintain cellular homeostasis, chronic activation of the UPR, known as ER stress, leads to sustained changes in cellular function. A growing body of literature points to ER stress in diverse cardioregulatory systems, including the brain, kidney and vasculature, as central to the development of hypertension. Here, these recent findings from essential and obesity-related forms of hypertension are highlighted in an integrative manner with discussion into potential upstream causes and downstream consequences of ER stress. Given that hypertension is a leading medical and socioeconomic global challenge, emerging findings suggest that targeting ER stress may represent a viable strategy for the treatment of hypertensive disease.

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