Int. J. Mol. Sci. 2016, 17(2), 192; doi:10.3390/ijms17020192
Pharmacological Modulators of Endoplasmic Reticulum Stress in Metabolic Diseases
Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, Korea University, Seoul 152-703, Korea
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Author to whom correspondence should be addressed.
Academic Editor: Masato Matsuoka
Received: 26 December 2015 / Revised: 20 January 2016 / Accepted: 27 January 2016 / Published: 1 February 2016
(This article belongs to the Special Issue Modulators of Endoplasmic Reticulum Stress)
Abstract
The endoplasmic reticulum (ER) is the principal organelle responsible for correct protein folding, a step in protein synthesis that is critical for the functional conformation of proteins. ER stress is a primary feature of secretory cells and is involved in the pathogenesis of numerous human diseases, such as certain neurodegenerative and cardiometabolic disorders. The unfolded protein response (UPR) is a defense mechanism to attenuate ER stress and maintain the homeostasis of the organism. Two major degradation systems, including the proteasome and autophagy, are involved in this defense system. If ER stress overwhelms the capacity of the cell’s defense mechanisms, apoptotic death may result. This review is focused on the various pharmacological modulators that can protect cells from damage induced by ER stress. The possible mechanisms for cytoprotection are also discussed. View Full-TextKeywords:
endoplasmic reticulum stress; unfolded protein response; AMPK-activated protein kinase; glucagon-like peptide-1; peroxisome proliferator-activated receptors; angiotensin II type 1 receptor blockers
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Jung, T.W.; Choi, K.M. Pharmacological Modulators of Endoplasmic Reticulum Stress in Metabolic Diseases. Int. J. Mol. Sci. 2016, 17, 192.
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