Review
Version 1
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Endoplasmic Reticulum Stress in Metabolic Disorders
Version 1
: Received: 17 May 2018 / Approved: 21 May 2018 / Online: 21 May 2018 (08:09:59 CEST)
A peer-reviewed article of this Preprint also exists.
Ghemrawi, R.; Battaglia-Hsu, S.-F.; Arnold, C. Endoplasmic Reticulum Stress in Metabolic Disorders. Cells 2018, 7, 63, doi:10.3390/cells7060063. Ghemrawi, R.; Battaglia-Hsu, S.-F.; Arnold, C. Endoplasmic Reticulum Stress in Metabolic Disorders. Cells 2018, 7, 63, doi:10.3390/cells7060063.
Abstract
Metabolic disorders have become among the most serious threats to human health, leading to severe chronic diseases such as obesity, type 2 diabetes, non-alcoholic fatty liver disease, as well as cardiovascular diseases. Interestingly, despite the fact that each of these maladies has different physiological and clinical symptoms, they appear to share certain pathological traits such as intracellular stress and inflammation induced by metabolic derangements stemmed from over nutrition frequently aggravated by modern sedentary life style. These modern ways of living inundate cells and organs with saturating levels of sugar and fat, leading to glycotoxicity and lipotoxicity that induce intracellular stress signaling ranging from oxidative to ER stress response to cope with the metabolic insults [1]. In this review, we discuss the roles played by cellular stress and its responses in shaping metabolic disorders. We have summarized here current mechanistic insights explaining the pathogenesis of these disorders. These are followed by a discussion of the latest therapies targeting the stress response pathways.
Keywords
endoplasmic reticulum stress; metabolic disorders; unfolded protein response; inflammation; lipotoxicity; glucotoxicity; therapy
Subject
Biology and Life Sciences, Immunology and Microbiology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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