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General Nutritional Considerations for Chronic Hyperglycemia—Type 2 Diabetes
Published in Robert Fried, Richard M. Carlton, Type 2 Diabetes, 2018
Robert Fried, Richard M. Carlton
When a cell starts to sense stress, a metaphoric “red light” signals slowing down the production of proteins. This process, which is known as the “endoplasmic reticulum stress response,” is abnormally active in the liver of obese individuals, where it contributes to the development of hyperglycemia. The endoplasmic reticulum is a structure within the cell that functions as a protein factory.
Childhood ILD
Published in Muhunthan Thillai, David R Moller, Keith C Meyer, Clinical Handbook of Interstitial Lung Disease, 2017
Disease is due to gain of function mutations. Kindreds with a range of age-related presentations have been described (above). Sp-C chILD is part of the differential diagnosis of RSV bronchiolitis which fails to resolve. Although in the largest series, empirical treatment with systemic corticosteroids, hydroxychloroquine and azithromycin is associated with a good prognosis (3), fatalities are well described. Very prolonged survival with good lung function with just intermittent hydroxychloroquine therapy has been described (41). Interestingly, a Japanese kindred just presenting with UIP in adult life, although containing one child with asymptomatic radiological abnormalities has been described (42). Endoplasmic reticulum stress (BiP, IRE1α, cleaved Caspase-3) was reported to be increased in vitro by the mutant protein. Finding the reasons why the presentation of an inherited abnormality may be delayed may offer avenues for the discovery of new treatments.
Bioinformatics analysis of the endoplasmic reticulum stress-related prognostic model and immune cell infiltration in acute myeloid leukemia
Published in Hematology, 2023
Mengya Pan, Junjie Zhou, Changqing Jiao, Jian Ge
Endoplasmic reticulum stress is an imbalance in ER homeostasis characterized by the accumulation of unfolded or misfolded proteins and alterations in the Ca2+ concentration. To alleviate the damage caused by endoplasmic reticulum stress, cells relieve ER stress through biological processes such as the unfolded protein response (UPR), endoplasmic reticulum-associated protein degradation (ERAD), and autophagosome formation [3]. Inositol requiring enzyme 1 (IRE1), protein kinase R-like ER kinase (PERK) and activating transcription factor 6 (ATF6) mediate three classic UPR pathways and play an essential role in relieving ERS and maintaining the homeostasis of the cellular environment [4]. In the absence of endoplasmic reticulum stress, these three sensors are in an inactive state due to their binding to the molecular chaperone protein named glucose-regulated protein 78 (GRP78/BiP) [5]. When ER stress occurs, unfolded proteins or misfolded proteins competitively bind to GRP78/BiP proteins such that GRP78/BiP dissociates from IRE1, PRKR and ATF6, activating downstream signaling pathways [5]. Inhibition of the UPR-mediated pro-survival pathway and induction of the persistent ERS-mediated pro-death pathway are two approaches for ER stress-related antitumor therapy.
Bicyclol alleviates high-fat diet-induced hepatic ER stress- and autophagy-associated non-alcoholic fatty liver disease/non-alcoholic steatohepatitis in mice
Published in Drug Development and Industrial Pharmacy, 2022
Shu Jia, Lianyu Jin, Xiaoyan Cheng, Jingyi Wu, Xiaokun Yao, Jingping Shao, Congcong Zhang, Danwei Cen, Bin Cheng, Jing Wang, Lei Chen, Xiaomin Yao
Endoplasmic reticulum stress is caused by the accumulation of unfolded or misfolded proteins, or changes in the Ca2+ concentration of the internal environment due to various reasons such as nutrient deficiencies, toxin stimulation, and sustained oxidative stress stimulation, resulting in an imbalance in the ER structure and function [17]. The theory of ‘multiple blows’ proposed recently emphasizes the roles of ER stress in the development of NASH [18]. ER stress and its mediated apoptosis are involved in the development of numerous liver diseases [19,20]. In a previous study, sustained and irreversible ER stress activated a number of intracellular signaling pathways associated with the development of NASH pathology, leading to a series of pathological changes, such as liver cell steatosis, inflammatory response, and cell death [21]. In addition, ER stress is also a potent trigger of autophagy, a self-degradative process with an adaptive function [22]. Research has shown that autophagy is involved in the pathogenesis of NAFLD and NASH progression to liver fibrosis [23]. However, no studies on the effect of bicyclol on hepatic autophagy during NASH have been published. Therefore, in-depth investigations on the related mechanisms are required.
Atorvastatin reduces alcohol-induced endoplasmic reticulum stress in AC16 cardiomyocytes
Published in Scandinavian Cardiovascular Journal, 2019
Ning Li, Chengyan Wen, Pinghe Huang, Yang Tao, Feng Jin, Xin Liu
Alcoholic cardiomyopathy (ACM) is a non-ischemic dilated heart muscle condition caused by heavy, chronic ethanol consumption. Its major clinical manifestations are cardiac enlargement, cardiac insufficiency, and arrhythmia [1]. Studies have shown that ACM pathogenesis involves several mechanisms at different layers and levels. These include the ethanol metabolic pathway, nutritional imbalance, oxidative stress, cell necrosis and apoptosis, and calcium dyshomeostasis [2,3]. Some studies have also shown that in ACM patients, dyslipidemia is very common, and statins are the most commonly used therapeutic agents for dyslipidemia. In recent years, increased attention has been given to the role of endoplasmic reticulum stress (ERS) in ACM pathogenesis. Previous studies mainly focused on the effects of ERS on the liver, kidney, nervous system, pancreas, and certain types of tumors [4,5]. In contrast, relatively few studies have examined the effects of ERS on cardiomyocytes or ACM cell models.