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Open AccessJournal ArticleDOI

An Involvement of Oxidative Stress in Endoplasmic Reticulum Stress and Its Associated Diseases

TLDR
The endoplasmic reticulum is the major site of calcium storage and protein folding, and Alterations in the oxidative environment of the ER and also intra-ER Ca2+ cause the production of ER stress-induced reactive oxygen species (ROS).
Abstract
The endoplasmic reticulum (ER) is the major site of calcium storage and protein folding. It has a unique oxidizing-folding environment due to the predominant disulfide bond formation during the process of protein folding. Alterations in the oxidative environment of the ER and also intra-ER Ca2+ cause the production of ER stress-induced reactive oxygen species (ROS). Protein disulfide isomerases, endoplasmic reticulum oxidoreductin-1, reduced glutathione and mitochondrial electron transport chain proteins also play crucial roles in ER stress-induced production of ROS. In this article, we discuss ER stress-associated ROS and related diseases, and the current understanding of the signaling transduction involved in ER stress.

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Citations
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Journal ArticleDOI

The Role of Oxidative Stress in Neurodegenerative Diseases

TL;DR: The role of oxidative stress in the pathophysiology of neurodegenerative diseases and in vivo measurement of an index of damage by oxidative stress are discussed and future directions will be outlined.
Journal ArticleDOI

Role of ROS and RNS Sources in Physiological and Pathological Conditions

TL;DR: The most recent data, besides confirming the mitochondrial role in tissue oxidative stress and protection, show interplay between mitochondria and other ROS cellular sources, so that activation of one can lead to activation of other sources.
Journal ArticleDOI

Reactive oxygen species and cancer paradox: To promote or to suppress?

TL;DR: This review focuses on the current understanding of the tumor promoting and the tumor suppressive functions of ROS, and highlights the potential mechanism(s) involved, and sheds light on a very novel and an actively growing field of ROS‐dependent cell death mechanism referred to as ferroptosis.
Journal ArticleDOI

Endoplasmic Reticulum Stress and Associated ROS

TL;DR: Persistent ER stress and protein misfolding-initiated ROS cascades and their significant roles in the pathogenesis of multiple human disorders, including neurodegenerative diseases, diabetes mellitus, atherosclerosis, inflammation, ischemia, and kidney and liver diseases are reviewed.
Journal ArticleDOI

Oxidative Stress in Aging Human Skin

TL;DR: In this review the overall effects of oxidative stress are discussed as well as the sources of ROS including the mitochondrial ETC, peroxisomal and ER localized proteins, the Fenton reaction, and such enzymes as cyclooxygenase, lipoxygenases, xanthine oxidases, and NADPH oxidases.
References
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Journal ArticleDOI

How mitochondria produce reactive oxygen species.

TL;DR: The description outlined here facilitates the understanding of factors that favour mitochondrial ROS production and develops better methods to measure mitochondrial O2•− and H2O2 formation in vivo, as uncertainty about these values hampers studies on the role of mitochondrial ROS in pathological oxidative damage and redox signalling.
Journal ArticleDOI

An Integrated Stress Response Regulates Amino Acid Metabolism and Resistance to Oxidative Stress

TL;DR: A signaling pathway initiated by eIF2alpha phosphorylation protects cells against metabolic consequences of ER oxidation by promoting the linked processes of amino acid sufficiency and resistance to oxidative stress.
Journal ArticleDOI

Oxidized redox state of glutathione in the endoplasmic reticulum

TL;DR: Results suggest that the demonstrated preferential transport of GSSG compared to GSH into the ER lumen may contribute to this redox compartmentation.
Journal ArticleDOI

Advanced oxidation protein products as a novel marker of oxidative stress in uremia

TL;DR: The measurement of AOPP is proposed as a reliable marker to estimate the degree of oxidant-mediated protein damage in uremic patients and to predict the potential efficacy of therapeutic strategies aimed at reducing such an oxidative stress.
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