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Journal articles on the topic 'Endoplasmic reticulum stress'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

BANHEGYI, G., P. BAUMEISTER, A. BENEDETTI, et al. "Endoplasmic Reticulum Stress." Annals of the New York Academy of Sciences 1113, no. 1 (2007): 58–71. http://dx.doi.org/10.1196/annals.1391.007.

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2

Schröder, M. "Endoplasmic reticulum stress responses." Cellular and Molecular Life Sciences 65, no. 6 (2007): 862–94. http://dx.doi.org/10.1007/s00018-007-7383-5.

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3

Hu, Yanan, Wenhao Yang, Liang Xie, Tao Liu, Hanmin Liu, and Bin Liu. "Endoplasmic reticulum stress and pulmonary hypertension." Pulmonary Circulation 10, no. 1 (2020): 204589401990012. http://dx.doi.org/10.1177/2045894019900121.

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Pulmonary hypertension is a fatal disease of which pulmonary vasculopathy is the main pathological feature resulting in the mean pulmonary arterial pressure higher than 25 mmHg. Moreover, pulmonary hypertension remains a tough problem with unclear molecular mechanisms. There have been dozens of studies about endoplasmic reticulum stress during the onset of pulmonary hypertension in patients, suggesting that endoplasmic reticulum stress may have a critical effect on the pathogenesis of pulmonary hypertension. The review aims to summarize the rationale to elucidate the role of endoplasmic reticu

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4

Koch, G., M. Smith, D. Macer, P. Webster, and R. Mortara. "Endoplasmic reticulum contains a common, abundant calcium-binding glycoprotein, endoplasmin." Journal of Cell Science 86, no. 1 (1986): 217–32. http://dx.doi.org/10.1242/jcs.86.1.217.

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The most abundant protein in microsomal membrane preparations from mammalian cells has been identified as a 100 X 10(3) Mr concanavalin A-binding glycoprotein. The glycosyl moiety of the glycoprotein is completely sensitive to endoglycosidase H, suggesting a predominantly endoplasmic reticulum localization in the cell. Using a monospecific antibody it was shown by binding and immunofluorescence studies that the glycoprotein is intracellular. Immunoelectron microscopy showed that the glycoprotein was at least 100 times more concentrated in the endoplasmic reticulum than in any other cellular or

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5

Das, Swapan K., Winston S. Chu, Ashis K. Mondal, et al. "Effect of pioglitazone treatment on endoplasmic reticulum stress response in human adipose and in palmitate-induced stress in human liver and adipose cell lines." American Journal of Physiology-Endocrinology and Metabolism 295, no. 2 (2008): E393—E400. http://dx.doi.org/10.1152/ajpendo.90355.2008.

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Obesity and elevated cytokine secretion result in a chronic inflammatory state and may cause the insulin resistance observed in type 2 diabetes. Recent studies suggest a key role for endoplasmic reticulum stress in hepatocytes and adipocytes from obese mice, resulting in reduced insulin sensitivity. To address the hypothesis that thiazolidinediones, which improve peripheral insulin sensitivity, act in part by reducing the endoplasmic reticulum stress response, we tested subcutaneous adipose tissue from 20 obese volunteers treated with pioglitazone for 10 wk. We also experimentally induced endo

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6

Groenendyk, Jody, Xiao Fan, Zhenling Peng, Lukasz Kurgan, and Marek Michalak. "Endoplasmic reticulum and the microRNA environment in the cardiovascular system." Canadian Journal of Physiology and Pharmacology 97, no. 6 (2019): 515–27. http://dx.doi.org/10.1139/cjpp-2018-0720.

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Stress responses are important to human physiology and pathology, and the inability to adapt to cellular stress leads to cell death. To mitigate cellular stress and re-establish homeostasis, cells, including those in the cardiovascular system, activate stress coping response mechanisms. The endoplasmic reticulum, a component of the cellular reticular network in cardiac cells, mobilizes so-called endoplasmic reticulum stress coping responses, such as the unfolded protein response. MicroRNAs play an important part in the maintenance of cellular and tissue homeostasis, perform a central role in t

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7

Hadley, Gina, Ain A. Neuhaus, Yvonne Couch, et al. "The role of the endoplasmic reticulum stress response following cerebral ischemia." International Journal of Stroke 13, no. 4 (2017): 379–90. http://dx.doi.org/10.1177/1747493017724584.

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Background Cornu ammonis 3 (CA3) hippocampal neurons are resistant to global ischemia, whereas cornu ammonis (CA1) 1 neurons are vulnerable. Hamartin expression in CA3 neurons mediates this endogenous resistance via productive autophagy. Neurons lacking hamartin demonstrate exacerbated endoplasmic reticulum stress and increased cell death. We investigated endoplasmic reticulum stress responses in CA1 and CA3 regions following global cerebral ischemia, and whether pharmacological modulation of endoplasmic reticulum stress or autophagy altered neuronal viability . Methods In vivo: male Wistar ra

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8

HAN, Sevtap, Mecit Orhan ULUDAĞ, and Emine DEMİREL YILMAZ. "Endoplasmic Reticulum Stress and Hypertension." Turkiye Klinikleri Journal of Internal Medicine 4, no. 3 (2019): 147–53. http://dx.doi.org/10.5336/intermed.2019-65618.

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9

Martinez, Alexis, Cristian M. Lamaizon, Cristian Valls, et al. "c-Abl Phosphorylates MFN2 to Regulate Mitochondrial Morphology in Cells under Endoplasmic Reticulum and Oxidative Stress, Impacting Cell Survival and Neurodegeneration." Antioxidants 12, no. 11 (2023): 2007. http://dx.doi.org/10.3390/antiox12112007.

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The endoplasmic reticulum is a subcellular organelle key in the control of synthesis, folding, and sorting of proteins. Under endoplasmic reticulum stress, an adaptative unfolded protein response is activated; however, if this activation is prolonged, cells can undergo cell death, in part due to oxidative stress and mitochondrial fragmentation. Here, we report that endoplasmic reticulum stress activates c-Abl tyrosine kinase, inducing its translocation to mitochondria. We found that endoplasmic reticulum stress-activated c-Abl interacts with and phosphorylates the mitochondrial fusion protein

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10

Li, Yina, Mingyang Li, Shi Feng, et al. "Ferroptosis and endoplasmic reticulum stress in ischemic stroke." Neural Regeneration Research 19, no. 3 (2023): 611–18. http://dx.doi.org/10.4103/1673-5374.380870.

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Abstract Ferroptosis is a form of non-apoptotic programmed cell death, and its mechanisms mainly involve the accumulation of lipid peroxides, imbalance in the amino acid antioxidant system, and disordered iron metabolism. The primary organelle responsible for coordinating external challenges and internal cell demands is the endoplasmic reticulum, and the progression of inflammatory diseases can trigger endoplasmic reticulum stress. Evidence has suggested that ferroptosis may share pathways or interact with endoplasmic reticulum stress in many diseases and plays a role in cell survival. Ferropt

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11

Dai, R. Y., S. K. Chen, D. M. Yan, et al. "PI3K/Akt Promotes GRP78 Accumulation and Inhibits Endoplasmic Reticulum Stress-Induced Apoptosis in HEK293 Cells." Folia Biologica 56, no. 2 (2010): 37–46. http://dx.doi.org/10.14712/fb2010056020037.

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The potential pro-survival role of phosphatidylinositol 3-kinase (PI3K)/Akt during endoplasmic reticulum stress has been well-characterized. However, the detailed mechanisms remain largely unknown. Here, we showed that PI3K/Akt inhibition promoted endoplasmic reticulum stress-induced apoptosis in a glucose-regulated protein 78 (GRP78)-dependent manner. During endoplasmic reticulum stress, high levels of Akt phosphorylation were sustained for at least 18 h in HEK293 cells. Importantly, PI3K/Akt enhanced GRP78 accumulation through increasing its stability following endoplasmic reticulum stress.

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12

Yang, Wei, and Wulf Paschen. "Unfolded protein response in brain ischemia: A timely update." Journal of Cerebral Blood Flow & Metabolism 36, no. 12 (2016): 2044–50. http://dx.doi.org/10.1177/0271678x16674488.

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Folding and processing newly synthesized proteins are vital functions of the endoplasmic reticulum that are sensitive to a variety of stress conditions. The unfolded protein response is activated to restore endoplasmic reticulum function impaired by stress. While we know that brain ischemia impairs endoplasmic reticulum function, the role of unfolded protein response activation in post-ischemic recovery of neurologic function is only beginning to emerge. Here, we summarize what is known about endoplasmic reticulum stress and unfolded protein response in brain ischemia and discuss recent findin

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13

Yang, Yong, Hao Peng, Danni Meng, et al. "Stress Management: How the Endoplasmic Reticulum Mitigates Protein Misfolding and Oxidative Stress by the Dual Role of Glutathione Peroxidase 8." Biomolecules 15, no. 6 (2025): 847. https://doi.org/10.3390/biom15060847.

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The endoplasmic reticulum mediates essential processes such as protein folding, transport, and post-translational modifications. Disruptions in endoplasmic reticulum function can lead to the accumulation of unfolded or misfolded proteins, initiating endoplasmic reticulum stress. This stress activates the unfolded protein response, a multifaceted signaling pathway aimed at restoring proteostasis, which is crucial for cellular survival and fate determination. This review summarizes the current knowledge of three major branches of the unfolded protein response: the IRE1, PERK, and ATF6 signaling

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14

Zhou, Long-Xia, An-Ning Yang, Jiu-Kai Chen та ін. "Endoplasmic reticulum oxidoreductin 1α mediates homocysteine-induced hepatocyte endoplasmic reticulum stress". World Chinese Journal of Digestology 22, № 34 (2014): 5228. http://dx.doi.org/10.11569/wcjd.v22.i34.5228.

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15

Liang, Wu-Lin, Meng-Ru Cai, Ming-Qian Zhang, et al. "Chinese Herbal Medicine Alleviates Myocardial Ischemia/Reperfusion Injury by Regulating Endoplasmic Reticulum Stress." Evidence-Based Complementary and Alternative Medicine 2021 (December 7, 2021): 1–17. http://dx.doi.org/10.1155/2021/4963346.

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Myocardial ischemia/reperfusion injury is the main cause of increased mortality and disability in cardiovascular diseases. The injury involves many pathological processes, such as oxidative stress, calcium homeostasis imbalance, inflammation, and energy metabolism disorders, and these pathological stimuli can activate endoplasmic reticulum stress. In the early stage of ischemia, endoplasmic reticulum stress alleviates the injury as an adaptive survival response, but the long-term stress on endoplasmic reticulum amplifies oxidative stress, inflammation, and calcium overload to accelerate cell d

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16

Alam, Rashedul, Mohammad Mamun Ur Rashid, Mohammad Fazlul Kabir, and Hyung-Ryong Kim. "Endoplasmic reticulum stress and organoids." Organoid 1 (January 31, 2021): e3. http://dx.doi.org/10.51335/organoid.2021.1.e3.

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Organoids represent an advanced tool in cell biology and have redefined biomedical research. Organoids are ideal for studies of biological processes, pharmacological studies, and therapeutic research to imitate pathological processes and preserve genetic integrity. The endoplasmic reticulum (ER) is the central organelle responsible for protein folding, post-translational adaptations, and membrane and luminal protein transportation. ER stress is a disorder influenced by a range of physiological and pathological causes, such as nutrient deficiency, impaired glycosylation, calcium depletion, oxid

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17

CHANG, YanZhong, PeiNa WANG, and YuanYuan LIU. "Ferroptosis and endoplasmic reticulum stress." SCIENTIA SINICA Vitae 51, no. 2 (2020): 126–34. http://dx.doi.org/10.1360/ssv-2020-0116.

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18

Kim, Mi Kyung, and Keun Gyu Park. "Endoplasmic Reticulum Stress and Diabetes." Journal of Korean Endocrine Society 23, no. 1 (2008): 1. http://dx.doi.org/10.3803/jkes.2008.23.1.1.

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19

Yadav, Raj Kumar, Soo-Wan Chae, Hyung-Ryong Kim, and Han Jung Chae. "Endoplasmic Reticulum Stress and Cancer." Journal of Cancer Prevention 19, no. 2 (2014): 75–88. http://dx.doi.org/10.15430/jcp.2014.19.2.75.

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20

Zhou, Junzhi, Beibei Mao, Qi Zhou, et al. "Endoplasmic reticulum stress activates telomerase." Aging Cell 13, no. 1 (2013): 197–200. http://dx.doi.org/10.1111/acel.12161.

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21

Crouser, Elliott D. "Sepsis-Induced Endoplasmic Reticulum Stress." Critical Care Medicine 44, no. 8 (2016): 1626–27. http://dx.doi.org/10.1097/ccm.0000000000001694.

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22

Hotamisligil, Gökhan S. "Endoplasmic reticulum stress and atherosclerosis." Nature Medicine 16, no. 4 (2010): 396–99. http://dx.doi.org/10.1038/nm0410-396.

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23

Minchenko, DO, KI Kubaĭchuk, OV Hubenia, et al. "Endoplasmic reticulum stress and angiogenesis." Fiziolohichnyĭ zhurnal 59, no. 4 (2013): 93–106. http://dx.doi.org/10.15407/fz59.04.093.

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24

Yorimitsu, Tomohiro, Usha Nair, Zhifen Yang, and Daniel J. Klionsky. "Endoplasmic Reticulum Stress Triggers Autophagy." Journal of Biological Chemistry 281, no. 40 (2006): 30299–304. http://dx.doi.org/10.1074/jbc.m607007200.

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25

Khan, Mohammad Moshahid, Weng-Lang Yang, and Ping Wang. "ENDOPLASMIC RETICULUM STRESS IN SEPSIS." Shock 44, no. 4 (2015): 294–304. http://dx.doi.org/10.1097/shk.0000000000000425.

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26

SATO, Masao, and Shinya SUZUKI. "Endoplasmic Reticulum Stress and Metallothionein." YAKUGAKU ZASSHI 127, no. 4 (2007): 703–8. http://dx.doi.org/10.1248/yakushi.127.703.

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27

Li, Jianze, Brenda Lee, and Amy S. Lee. "Endoplasmic Reticulum Stress-induced Apoptosis." Journal of Biological Chemistry 281, no. 11 (2006): 7260–70. http://dx.doi.org/10.1074/jbc.m509868200.

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28

Kraskiewicz, Honorata, and Una FitzGerald. "InterfERing with endoplasmic reticulum stress." Trends in Pharmacological Sciences 33, no. 2 (2012): 53–63. http://dx.doi.org/10.1016/j.tips.2011.10.002.

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29

Bettigole, Sarah E., and Laurie H. Glimcher. "Endoplasmic Reticulum Stress in Immunity." Annual Review of Immunology 33, no. 1 (2015): 107–38. http://dx.doi.org/10.1146/annurev-immunol-032414-112116.

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30

Clarke, Hanna J., Joseph E. Chambers, Elizabeth Liniker, and Stefan J. Marciniak. "Endoplasmic Reticulum Stress in Malignancy." Cancer Cell 25, no. 5 (2014): 563–73. http://dx.doi.org/10.1016/j.ccr.2014.03.015.

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31

Hama, Taketsugu, Koichi Nakanishi, Hironobu Mukaiyama, Masashi Sato, Yuko Shima, and Norishige Yoshikawa. "Cyclosporine and endoplasmic reticulum stress." Nihon Shoni Jinzobyo Gakkai Zasshi 27, no. 1 (2014): 13–18. http://dx.doi.org/10.3165/jjpn.27.13.

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32

TAKAHASHI, RYOSUKE, YUZURU IMAI, NOBUTAKA HATTORI, and YOSHIKUNI MIZUNO. "Parkin and Endoplasmic Reticulum Stress." Annals of the New York Academy of Sciences 991, no. 1 (2006): 101–6. http://dx.doi.org/10.1111/j.1749-6632.2003.tb07467.x.

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33

Zhou, Huiping, Lixin Sun, Jian Xiao, et al. "Endoplasmic Reticulum Stress and Atherosclerosis." Current Hypertension Reviews 6, no. 1 (2010): 66–71. http://dx.doi.org/10.2174/157340210790231744.

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34

Adolph, Timon-Eric, Lukas Niederreiter, Richard S. Blumberg, and Arthur Kaser. "Endoplasmic Reticulum Stress and Inflammation." Digestive Diseases 30, no. 4 (2012): 341–46. http://dx.doi.org/10.1159/000338121.

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35

Miyata, Toshio, Reiko Inagi, Satoshi Sugiyama, and Nobuteru Usuda. "Serpinopathy and endoplasmic reticulum stress." Medical Molecular Morphology 38, no. 2 (2005): 73–78. http://dx.doi.org/10.1007/s00795-004-0281-0.

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36

Papp, Sylvia, Xiaochu Zhang, Eva Szabo, Marek Michalak, and Michal Opas. "Expression of Endoplasmic Reticulum Chaperones in Cardiac Development." Open Cardiovascular Medicine Journal 2, no. 1 (2008): 31–35. http://dx.doi.org/10.2174/1874192400802010031.

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To determine if cardiogenesis causes endoplasmic reticulum stress, we examined chaperone expression. Many cardiac pathologies cause activation of the fetal gene program, and we asked the reverse: could activation of the fetal gene program during development induce endoplasmic reticulum stress/chaperones? We found stress related chaperones were more abundant in embryonic compared to adult hearts, indicating endoplasmic reticulum stress during normal cardiac development. To determine the degree of stress, we investigated endoplasmic reticulum stress pathways during cardiogenesis. We detected hig

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37

Nugraha, Wahyu Cahyana. "GRP78 as a Target for Prevention of Age-related Cataract By Regulation of Reticulum Endoplasmic Stress." INTERNATIONAL JOURNAL OF INNOVATIVE RESEARCH IN MULTIDISCIPLINARY EDUCATION 02, no. 01 (2023): 26–30. https://doi.org/10.5281/zenodo.7573497.

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Cataract is the most common causes of blindness worldwide. The most common kind of cataract is age-related cataract. Measures to prevent the development of cataracts are urgently needed. Significant data suggests that increased endoplasmic reticulum stress is a significant role in cataract development. The goal of this review is to investigate the involvement of endoplasmic reticulum as a factor in cataracts caused by the buildup of unfolded proteins from lens epithelial cells. GRP78 is one of the key signs of endoplasmic reticulum stress, and it promotes the UPR to limit the increase in unfol

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38

Correia de Sousa, Marta, Etienne Delangre, Miranda Türkal, Michelangelo Foti, and Monika Gjorgjieva. "Endoplasmic Reticulum Stress in Renal Cell Carcinoma." International Journal of Molecular Sciences 24, no. 5 (2023): 4914. http://dx.doi.org/10.3390/ijms24054914.

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The endoplasmic reticulum is an organelle exerting crucial functions in protein production, metabolism homeostasis and cell signaling. Endoplasmic reticulum stress occurs when cells are damaged and the capacity of this organelle to perform its normal functions is reduced. Subsequently, specific signaling cascades, together forming the so-called unfolded protein response, are activated and deeply impact cell fate. In normal renal cells, these molecular pathways strive to either resolve cell injury or activate cell death, depending on the extent of cell damage. Therefore, the activation of the e

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39

Dong, Yunzhou, Conrad Fernandes, Yanjun Liu, et al. "Role of endoplasmic reticulum stress signalling in diabetic endothelial dysfunction and atherosclerosis." Diabetes and Vascular Disease Research 14, no. 1 (2016): 14–23. http://dx.doi.org/10.1177/1479164116666762.

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It is well established that diabetes mellitus accelerates atherosclerotic vascular disease. Endothelial injury has been proposed to be the initial event in the pathogenesis of atherosclerosis. Endothelium not only acts as a semi-selective barrier but also serves physiological and metabolic functions. Diabetes or high glucose in circulation triggers a series of intracellular responses and organ damage such as endothelial dysfunction and apoptosis. One such response is high glucose-induced chronic endoplasmic reticulum stress in the endothelium. The unfolded protein response is an acute reaction

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40

HAN, Fang, Hong LIU, Bing XIAO, et al. "Endoplasmic reticulum stress and posttraumatic stress disorder." Advances in Psychological Science 25, no. 12 (2017): 2013. http://dx.doi.org/10.3724/sp.j.1042.2017.02013.

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41

Liu, Xiaoqing, Riaz Hussain, Khalid Mehmood, Zhaoxin Tang, Hui Zhang, and Ying Li. "Mitochondrial-Endoplasmic Reticulum Communication-Mediated Oxidative Stress and Autophagy." BioMed Research International 2022 (September 17, 2022): 1–12. http://dx.doi.org/10.1155/2022/6459585.

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Oxidative stress is an imbalance between free radicals and the antioxidant system causing overgeneration of free radicals (oxygen-containing molecules) ultimately leading to oxidative damage in terms of lipid peroxidation, protein denaturation, and DNA mutation. Oxidative stress can activate autophagy to alleviate oxidative damage and maintain normal physiological activities of cells by degrading damaged organelles or local cytoplasm. When oxidative stress is not eliminated by autophagy, it activates the apoptosis cascade. This review provides a brief summary of mitochondrial-endoplasmic retic

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42

Lucke-Wold, Brandon P., Ryan C. Turner, Aric F. Logsdon, et al. "Endoplasmic reticulum stress implicated in chronic traumatic encephalopathy." Journal of Neurosurgery 124, no. 3 (2016): 687–702. http://dx.doi.org/10.3171/2015.3.jns141802.

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OBJECT Chronic traumatic encephalopathy is a progressive neurodegenerative disease characterized by neurofibrillary tau tangles following repetitive neurotrauma. The underlying mechanism linking traumatic brain injury to chronic traumatic encephalopathy has not been elucidated. The authors investigate the role of endoplasmic reticulum stress as a link between acute neurotrauma and chronic neurodegeneration. METHODS The authors used pharmacological, biochemical, and behavioral tools to assess the role of endoplasmic reticulum stress in linking acute repetitive traumatic brain injury to the deve

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43

Guo, Shulong, Shaoya Wang, Youxiao Zeng та Qiaosheng Hu. "Stress-Associated Endoplasmic Reticulum Protein 1 Protected High Glucose-Induced Islet β Cells from Apoptosis by Attenuating Endoplasmic Reticulum Stress". Journal of Biomaterials and Tissue Engineering 9, № 12 (2019): 1731–38. http://dx.doi.org/10.1166/jbt.2019.2192.

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The incidence of type II diabetes caused by islet cell injury is increasing in recent years. Endoplasmic reticulum stress is one of the crucial causes of islet β cell damage, and stress-associated endoplasmic reticulum protein 1 (SERP1) could inhibit the occurrence and development of endoplasmic reticulum stress. But whether SERP1 could inhibit the damage of islet β cell caused by endoplasmic reticulum stress is unclear. In this study, we detected the levels of SERP1 and endoplasmic reticulum stress related proteins (p-PERK, p-Eif2 α, ATF-4 and CHOP) by western blotting. Next the lentivirus wa

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44

Han, Yiping, Shunsuke Watanabe, Hiroshi Shimada та Atsushi Sakamoto. "Dynamics of the leaf endoplasmic reticulum modulate β-glucosidase-mediated stress-activated ABA production from its glucosyl ester". Journal of Experimental Botany 71, № 6 (2019): 2058–71. http://dx.doi.org/10.1093/jxb/erz528.

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Abstract The phytohormone abscisic acid (ABA) is produced via a multistep de novo biosynthesis pathway or via single-step hydrolysis of inactive ABA-glucose ester (ABA-GE). The hydrolysis reaction is catalyzed by β-glucosidase (BG, or BGLU) isoforms localized to various organelles, where they become activated upon stress, but the mechanisms underlying this organelle-specific activation remain unclear. We investigated the relationship between the subcellular distribution and stress-induced activation of BGLU18 (BG1), an endoplasmic reticulum enzyme critical for abiotic stress responses, in Arab

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45

Buono, Lola, Simona Scalabrin, Marco De Iuliis, et al. "Mesenchymal Stem Cell-Derived Extracellular Vesicles Protect Human Corneal Endothelial Cells from Endoplasmic Reticulum Stress-Mediated Apoptosis." International Journal of Molecular Sciences 22, no. 9 (2021): 4930. http://dx.doi.org/10.3390/ijms22094930.

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Corneal endothelial dystrophy is a relevant cause of vision loss and corneal transplantation worldwide. In the present study, we analyzed the effect of mesenchymal stem cell (MSC)-derived extracellular vesicles (MSC-EVs) in an in vitro model of corneal dystrophy, characterized by endoplasmic reticulum stress. The effects of MSC-EVs were compared with those of serum-derived EVs, reported to display a pro-angiogenic activity. MSC-EVs were able to induce a significant down-regulation of the large majority of endoplasmic reticulum stress-related genes in human corneal endothelial cells after expos

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46

Mao, Yanting, Chenchen Wang, Xinyu Tian, et al. "Endoplasmic Reticulum Stress Contributes to Nociception via Neuroinflammation in a Murine Bone Cancer Pain Model." Anesthesiology 132, no. 2 (2020): 357–72. http://dx.doi.org/10.1097/aln.0000000000003078.

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Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background Prolonged endoplasmic reticulum stress has been identified in various diseases. Inflammatory mediators, which have been shown to induce endoplasmic reticulum stress in several studies, have been suggested to serve as the important modulators in pain development. In this study, the authors hypothesized that the endoplasmic reticulum stress triggered by inflammatory mediators contributed to pain development. Methods The authors used a male mouse model of bone cancer pain. The con

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47

Wang, Dong, Yuren Wei, Dieter Schmoll, Kenneth N. Maclean, and Michael J. Pagliassotti. "Endoplasmic Reticulum Stress Increases Glucose-6-Phosphatase and Glucose Cycling in Liver Cells." Endocrinology 147, no. 1 (2006): 350–58. http://dx.doi.org/10.1210/en.2005-1014.

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Impaired regulation of hepatic glucose production is a characteristic feature of the metabolic syndrome, a cluster of diseases that includes obesity, insulin resistance, type 2 diabetes, and cardiovascular disease. It has been proposed that sustained endoplasmic reticulum stress, which appears to occur in obesity and diabetes, modulates insulin action in the liver. In this study, we show that experimental induction of endoplasmic reticulum stress increases expression and activity of glucose-6-phosphatase and the capacity for glucose release and glucose cycling in primary rat hepatocytes and H4

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48

Marciniak, Stefan J. "Endoplasmic reticulum stress in lung disease." European Respiratory Review 26, no. 144 (2017): 170018. http://dx.doi.org/10.1183/16000617.0018-2017.

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Exposure to inhaled pollutants, including fine particulates and cigarette smoke is a major cause of lung disease in Europe. While it is established that inhaled pollutants have devastating effects on the genome, it is now recognised that additional effects on protein folding also drive the development of lung disease. Protein misfolding in the endoplasmic reticulum affects the pathogenesis of many diseases, ranging from pulmonary fibrosis to cancer. It is therefore important to understand how cells respond to endoplasmic reticulum stress and how this affects pulmonary tissues in disease. These

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49

Michalak, Marek, and Myung Chan Gye. "Endoplasmic reticulum stress in periimplantation embryos." Clinical and Experimental Reproductive Medicine 42, no. 1 (2015): 1. http://dx.doi.org/10.5653/cerm.2015.42.1.1.

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50

WANG, Ying, Ye XIONG, Yan SHANG, Qiang LI, and Chong BAI. "Endoplasmic reticulum stress and bronchial asthma." Academic Journal of Second Military Medical University 36, no. 1 (2015): 74. http://dx.doi.org/10.3724/sp.j.1008.2015.00074.

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