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The aftermath of the interplay between the endoplasmic reticulum stress response and redox signaling

Experimental & Molecular Medicine 2021년 53권 2호 p.151 ~ 167
Bhattarai Kashi Raj, Riaz Thoufiqul Alam, 김형령, 채한정,
소속 상세정보
 ( Bhattarai Kashi Raj ) - Jeonbuk National University School of Pharmacy
 ( Riaz Thoufiqul Alam ) - Chonbuk National University Medical School Department of Pharmacology
김형령 ( Kim Hyung-Ryong ) - Dankook University College of Dentistry
채한정 ( Chae Han-Jung ) - Jeonbuk National University School of Pharmacy

Abstract


The endoplasmic reticulum (ER) is an essential organelle of eukaryotic cells. Its main functions include protein synthesis, proper protein folding, protein modification, and the transportation of synthesized proteins. Any perturbations in ER function, such as increased demand for protein folding or the accumulation of unfolded or misfolded proteins in the ER lumen, lead to a stress response called the unfolded protein response (UPR). The primary aim of the UPR is to restore cellular homeostasis; however, it triggers apoptotic signaling during prolonged stress. The core mechanisms of the ER stress response, the failure to respond to cellular stress, and the final fate of the cell are not yet clear. Here, we discuss cellular fate during ER stress, cross talk between the ER and mitochondria and its significance, and conditions that can trigger ER stress response failure. We also describe how the redox environment affects the ER stress response, and vice versa, and the aftermath of the ER stress response, integrating a discussion on redox imbalance-induced ER stress response failure progressing to cell death and dynamic pathophysiological changes.

키워드

Cell biology; Mechanisms of disease

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