Endoplasmic Reticulum Stress in Cardiometabolic Disorders
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When endoplasmic reticulum (ER) homeostasis is disrupted, an adaptive signaling pathway, called the unfolded protein response (UPR) is activated to help ER cope with the stress. The UPR is an important signal transduction pathway, crucial for the survival and function of all cells. Recently, there has been a substantial progress made in understanding the molecular mechanisms of physiological UPR regulation and its role in the pathogenesis of many diseases including metabolic diseases. Studies using mouse models lacking or overexpressing the factors involved in ER stress signaling as well as work performed on humans have revealed the contribution of UPR to disease progression. This review focuses on the regulation of UPR signaling and its relevance in pathogenesis of metabolic diseases.
KeywordsER Stress UPR Obesity Diabetes Atherosclerosis NAFLD
I gratefully thank my mentor Ira Tabas, M.D., Ph.D. for his guidance, creativity and support and all the past & present members of the Tabas Lab. Funding is from American Heart Association Scientist Development Grant (11SDG5300022).
No potential conflict of interest relevant to this article was reported.
Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance
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