Abstract
Pathogenesis of atherosclerosis is a complex process involving several metabolic and signalling pathways. Accumulating evidence demonstrates that endoplasmic reticulum stress and associated apoptosis can be induced in the pathological conditions of atherosclerotic lesions and contribute to the disease progression. Notably, they may play a role in the development of vulnerable plaques that induce thrombosis and are therefore especially dangerous. Endoplasmic reticulum stress response is regulated by several signaling mechanisms that involve protein kinases and transcription factors. Some of these molecules can be regarded as potential therapeutic targets to improve treatment of atherosclerosis. In this review we will discuss the role of endoplasmic reticulum stress and apoptosis in atherosclerosis development in different cell types and summarize the current knowledge on potential therapeutic agents targeting molecules regulating these pathways and their possible use for anti-atherosclerotic therapy.
Highlights
Atherosclerosis is one of the most challenging problems of current medicine, being the primary cause of the development of cardiovascular diseases that account for the majority of fatal illnesses in developed countries [1]
The main source of cholesterol deposit in the arterial wall is the atherogenic fraction of low-density lipoprotein (LDL)
These results suggest that unfolded protein response (UPR) activation at early stages of atherosclerosis plays a protective role in response to stress induced by disturbed blood flow
Summary
Atherosclerosis is one of the most challenging problems of current medicine, being the primary cause of the development of cardiovascular diseases that account for the majority of fatal illnesses in developed countries [1]. The development of atherosclerotic lesion is associated with local inflammation and the recruitment of circulating immune cells Both resident arterial wall cells (such as pericytes and vascular smooth muscle cells) and infiltrated cells (such as macrophages) actively participate in the pathological process. The protein folding capacity of the ER can be saturated in various conditions, including ischemia, oxidative stress, disturbances of calcium homeostasis, accumulation of folding-defective proteins or enhanced expression of normal proteins [8]. These conditions can result in the development of ER stress
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