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      Oxidative Stress and the Kidney in the Space Environment

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          Abstract

          In space, the special conditions of hypogravity and exposure to cosmic radiation have substantial differences compared to terrestrial circumstances, and a multidimensional impact on the human body and human organ functions. Cosmic radiation provokes cellular and gene damage, and the generation of reactive oxygen species (ROS), leading to a dysregulation in the oxidants–antioxidants balance, and to the inflammatory response. Other practical factors contributing to these dysregulations in space environment include increased bone resorption, impaired anabolic response, and even difficulties in detecting oxidative stress in blood and urine samples. Enhanced oxidative stress affects mitochondrial and endothelial functions, contributes to reduced natriuresis and the development of hypertension, and may play an additive role in the formation of kidney stones. Finally, the composition of urine protein excretion is significantly altered, depicting possible tubular dysfunction.

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          Most cited references95

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          Biochemistry, physiology, and pathophysiology of NADPH oxidases in the cardiovascular system.

          The NADPH oxidase (Nox) enzymes are critical mediators of cardiovascular physiology and pathophysiology. These proteins are expressed in virtually all cardiovascular cells, and regulate such diverse functions as differentiation, proliferation, apoptosis, senescence, inflammatory responses and oxygen sensing. They target a number of important signaling molecules, including kinases, phosphatases, transcription factors, ion channels, and proteins that regulate the cytoskeleton. Nox enzymes have been implicated in many different cardiovascular pathologies: atherosclerosis, hypertension, cardiac hypertrophy and remodeling, angiogenesis and collateral formation, stroke, and heart failure. In this review, we discuss in detail the biochemistry of Nox enzymes expressed in the cardiovascular system (Nox1, 2, 4, and 5), their roles in cardiovascular cell biology, and their contributions to disease development.
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            Oxidative stress in angiogenesis and vascular disease.

            Despite the damaging effect on tissues at a high concentration, it has been gradually established that oxidative stress plays a positive role during angiogenesis. In adults, physiological or pathological angiogenesis is initiated by tissue demands for oxygen and nutrients, resulting in a hypoxia/reoxygenation cycle, which, in turn promotes the formation of reactive oxygen species (ROS). The ROS can be generated either endogenously, through mitochondrial electron transport chain reactions and nicotinamide adenine dinucleotide phosphate oxidase, or exogenously, resulting from exposure to environmental agents, such as ultraviolet or ionizing radiation. In many conditions, ROS promotes angiogenesis, either directly or via the generation of active oxidation products, including peroxidized lipids. The latter lipid metabolites are generated in excess during atherosclerosis, thereby linking atherogenic processes and pathological angiogenesis. Although the main mechanism of oxidative stress-induced angiogenesis involves hypoxia-inducible factor/vascular endothelial growth factor (VEGF) signaling, recent studies have identified several pathways that are VEGF-independent. This review aims to provide a summary of the past and present views on the role of oxidative stress as a mediator and modulator of angiogenesis, and to highlight newly identified mechanisms.
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              Mitochondrial dysfunction in the pathophysiology of renal diseases.

              Mitochondrial dysfunction has gained recognition as a contributing factor in many diseases. The kidney is a kind of organ with high energy demand, rich in mitochondria. As such, mitochondrial dysfunction in the kidney plays a critical role in the pathogenesis of kidney diseases. Despite the recognized importance mitochondria play in the pathogenesis of the diseases, there is limited understanding of various aspects of mitochondrial biology. This review examines the physiology and pathophysiology of mitochondria. It begins by discussing mitochondrial structure, mitochondrial DNA, mitochondrial reactive oxygen species production, mitochondrial dynamics, and mitophagy, before turning to inherited mitochondrial cytopathies in kidneys (inherited or sporadic mitochondrial DNA or nuclear DNA mutations in genes that affect mitochondrial function). Glomerular diseases, tubular defects, and other renal diseases are then discussed. Next, acquired mitochondrial dysfunction in kidney diseases is discussed, emphasizing the role of mitochondrial dysfunction in the pathogenesis of chronic kidney disease and acute kidney injury, as their prevalence is increasing. Finally, it summarizes the possible beneficial effects of mitochondrial-targeted therapeutic agents for treatment of mitochondrial dysfunction-mediated kidney injury-genetic therapies, antioxidants, thiazolidinediones, sirtuins, and resveratrol-as mitochondrial-based drugs may offer potential treatments for renal diseases.
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                Author and article information

                Journal
                Int J Mol Sci
                Int J Mol Sci
                ijms
                International Journal of Molecular Sciences
                MDPI
                1422-0067
                15 October 2018
                October 2018
                : 19
                : 10
                : 3176
                Affiliations
                [1 ]Department of Nephrology, Medical School, University of Ioannina, 45110 Ioannina, Greece; pavlakoup@ 123456gmail.com (P.P.); evangeldou@ 123456gmail.com (E.D.)
                [2 ]Division of Nephrology and Hypertension, 1st Department of Internal Medicine, AHEPA Hospital, School of Medicine, Aristotle University of Thessaloniki, 54636 Thessaloniki, Greece; st_roumeliotis@ 123456hotmail.com (S.R.); teleftheriadis@ 123456yahoo.com (T.E.)
                Author notes
                [* ]Correspondence: liakopul@ 123456otenet.gr
                [†]

                These authors contributed equally to this work.

                Author information
                https://orcid.org/0000-0001-9302-1633
                https://orcid.org/0000-0002-7564-2724
                Article
                ijms-19-03176
                10.3390/ijms19103176
                6214023
                30326648
                32b4b932-e0e9-4440-92dc-7c24fb7127c7
                © 2018 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 29 July 2018
                : 12 October 2018
                Categories
                Review

                Molecular biology
                cosmic radiation,microgravity,kidney,oxidative stress,space
                Molecular biology
                cosmic radiation, microgravity, kidney, oxidative stress, space

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