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- W2263704189 endingPage "193" @default.
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- W2263704189 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." @default.
- W2263704189 created "2016-06-24" @default.
- W2263704189 creator A5011643232 @default.
- W2263704189 creator A5064915726 @default.
- W2263704189 date "2016-02-01" @default.
- W2263704189 modified "2023-10-10" @default.
- W2263704189 title "The Role of Endoplasmic Reticulum Stress and Unfolded Protein Response in Atherosclerosis" @default.
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- W2263704189 doi "https://doi.org/10.3390/ijms17020193" @default.
- W2263704189 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4783927" @default.
- W2263704189 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26840309" @default.
- W2263704189 hasPublicationYear "2016" @default.
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