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Ting Xiao, Xiuci Liang, Hailan Liu, Feng Zhang, Wen Meng, and Fang Hu

Introduction Endoplasmic reticulum (ER) stress due to high fat diet (HFD) feeding or genetic obesity is associated with hepatic steatosis and insulin resistance ( Kammoun et al . 2009 , Yoshiuchi et al . 2009 , Ye et al . 2010 , Meng et

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Liping Luo, Wanxiang Jiang, Hui Liu, Jicheng Bu, Ping Tang, Chongyangzi Du, Zhipeng Xu, Hairong Luo, Bilian Liu, Bo Xiao, Zhiguang Zhou, and Feng Liu

ER stress, leading to UPR and impaired lipid homeostasis ( Ron & Walter 2007 , Rutkowski et al . 2008 , Walter & Ron 2011 ). While long-term HFD feeding and genetic obesity have been well-documented to induce chronic ER stress associated with

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Fabio Arturo Grieco, Andrea Alex Schiavo, Flora Brozzi, Jonas Juan-Mateu, Marco Bugliani, Piero Marchetti, and Décio L Eizirik

systems taking place during insulitis ( Eizirik et al. 2009 , 2012 , Santin & Eizirik 2013 , Floyel et al. 2015 ). Islets inflammation triggers endoplasmic reticulum (ER) stress in beta cells exacerbating inflammation and contributing to beta cell

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S Lortz, S Lenzen, and I Mehmeti

(Prdx4). On the other hand, the activation of the ER stress pathway, which may lead to apoptotic cell death, has also been associated to the fulminant ROS generation in the ER ( Malhotra et al . 2008 , Bhandary et al . 2012 , Cao & Kaufman 2014 ). To

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Sumaira Z Hasnain, Johannes B Prins, and Michael A McGuckin

reticulum (ER) stress in β-cell dysfunction in T2D. We first overview insulin biosynthesis and secretion, summarise the features of progression of diabetes. We then detail the significance of oxidative and ER stress in β-cell homeostasis and dysfunction

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Sun-Ji Park, Tae-Shin Kim, Choon-Keun Park, Sang-Hee Lee, Jin-Man Kim, Kyu-Sun Lee, In-kyu Lee, Jeen-Woo Park, Mark A Lawson, and Dong-Seok Lee

in ER stress through activation of the unfolded protein response (UPR). The UPR serves to alleviate ER stress, rescue ER homeostasis, and prevent cell death through the induction of ER chaperone expression, reduction of protein synthesis, and

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Penny Ahlstrom, Esther Rai, Suharto Chakma, Hee Ho Cho, Palanivel Rengasamy, and Gary Sweeney

2 diabetes and upon aging ( Zhang et al. 2016 , Moller et al. 2017 , Zhou et al. 2017 ). Until recently, the causative role of ER stress in promoting insulin resistance in skeletal muscle was much less studied than other tissues. However

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Kira Meyerovich, Fernanda Ortis, Florent Allagnat, and Alessandra K Cardozo

signaling pathways mediated by the action of three signaling proteins named inositol-requiring protein 1α (IRE1α), protein kinase RNA (PKR)-like ER kinase (PERK), and activating transcription factor 6 (ATF6) ( Walter & Ron 2011 ). Upon ER stress, IRE1α

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JaeSang Ko, Ji-Young Kim, Eun Jig Lee, and Jin Sook Yoon

ER lumen), unfolded proteins accumulate in the ER, reflecting cellular stress induced by multiple stimuli and pathological conditions ( Kim et al. 2008 ). Under this condition, the ER elicits an elaborate adaptive response known as the unfolded

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Jie Sun, Yan Liu, Jinhui Yu, Jin Wu, Wenting Gao, Liyuan Ran, Rujiao Jiang, Meihua Guo, Dongyu Han, Bo Liu, Ning Wang, Youwei Li, He Huang, Li Zeng, Ying Gao, Xin Li, and Yingjie Wu

of the body, the liver plays a central role in metabolic functions ( Bechmann et al. 2012 ). Abnormalities in the reciprocal regulation between autophagy and endoplasmic reticulum (ER) stress in the liver have been associated with overfeeding