For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
22
views
64
references
 Top references
cited by
28
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      81
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      The Impact of Oxidative Stress on the Bone System in Response to the Space Special Environment

      review-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The space special environment mainly includes microgravity, radiation, vacuum and extreme temperature, which seriously threatens an astronaut’s health. Bone loss is one of the most significant alterations in mammalians after long-duration habitation in space. In this review, we summarize the crucial roles of major factors—namely radiation and microgravity—in space in oxidative stress generation in living organisms, and the inhibitory effect of oxidative stress on bone formation. We discussed the possible mechanisms of oxidative stress-induced skeletal involution, and listed some countermeasures that have therapeutic potentials for bone loss via oxidative stress antagonism. Future research for better understanding the oxidative stress caused by space environment and the development of countermeasures against oxidative damage accordingly may facilitate human beings to live more safely in space and explore deeper into the universe.

          Related collections

          Most cited references64

          • Record: found
          • Abstract: found
          • Article: not found

          From estrogen-centric to aging and oxidative stress: a revised perspective of the pathogenesis of osteoporosis.

          Stavros C. Manolagas (2010)
          Estrogen deficiency has been considered the seminal mechanism of osteoporosis in both women and men, but epidemiological evidence in humans and recent mechanistic studies in rodents indicate that aging and the associated increase in reactive oxygen species (ROS) are the proximal culprits. ROS greatly influence the generation and survival of osteoclasts, osteoblasts, and osteocytes. Moreover, oxidative defense by the FoxO transcription factors is indispensable for skeletal homeostasis at any age. Loss of estrogens or androgens decreases defense against oxidative stress in bone, and this accounts for the increased bone resorption associated with the acute loss of these hormones. ROS-activated FoxOs in early mesenchymal progenitors also divert ss-catenin away from Wnt signaling, leading to decreased osteoblastogenesis. This latter mechanism may be implicated in the pathogenesis of type 1 and 2 diabetes and ROS-mediated adverse effects of diabetes on bone formation. Attenuation of Wnt signaling by the activation of peroxisome proliferator-activated receptor gamma by ligands generated from lipid oxidation also contributes to the age-dependent decrease in bone formation, suggesting a mechanistic explanation for the link between atherosclerosis and osteoporosis. Additionally, increased glucocorticoid production and sensitivity with advancing age decrease skeletal hydration and thereby increase skeletal fragility by attenuating the volume of the bone vasculature and interstitial fluid. This emerging evidence provides a paradigm shift from the "estrogen-centric" account of the pathogenesis of involutional osteoporosis to one in which age-related mechanisms intrinsic to bone and oxidative stress are protagonists and age-related changes in other organs and tissues, such as ovaries, accentuate them.
          Article 0 comments Cited 396 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Functional interaction between beta-catenin and FOXO in oxidative stress signaling.

            Marieke Essers, Lydia M M de Vries-Smits, Nick Barker … (2005)
            beta-Catenin is a multifunctional protein that mediates Wnt signaling by binding to members of the T cell factor (TCF) family of transcription factors. Here, we report an evolutionarily conserved interaction of beta-catenin with FOXO transcription factors, which are regulated by insulin and oxidative stress signaling. beta-Catenin binds directly to FOXO and enhances FOXO transcriptional activity in mammalian cells. In Caenorhabditis elegans, loss of the beta-catenin BAR-1 reduces the activity of the FOXO ortholog DAF-16 in dauer formation and life span. Association of beta-catenin with FOXO was enhanced in cells exposed to oxidative stress. Furthermore, BAR-1 was required for the oxidative stress-induced expression of the DAF-16 target gene sod-3 and for resistance to oxidative damage. These results demonstrate a role for beta-catenin in regulating FOXO function that is particularly important under conditions of oxidative stress.
            Article 0 comments Cited 208 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Oxidative stress antagonizes Wnt signaling in osteoblast precursors by diverting beta-catenin from T cell factor- to forkhead box O-mediated transcription.

              C. O’Brien, Lúcia Braz, Stavros C. Manolagas … (2007)
              We have elucidated that oxidative stress is a pivotal pathogenetic factor of age-related bone loss and strength in mice, leading to, among other changes, a decrease in osteoblast number and bone formation. To gain insight into the molecular mechanism by which oxidative stress exerts such adverse effects, we have tested the hypothesis that induction of the Forkhead box O (FoxO) transcription factors by reactive oxygen species may antagonize Wnt signaling, an essential stimulus for osteoblastogenesis. In support of this hypothesis, we report herein that the expression of FoxO target genes increases, whereas the expression of Wnt target genes decreases, with increasing age in C57BL/6 mice. Moreover, we show that in osteoblastic cell models, oxidative stress (exemplified by H(2)O(2)) promotes the association of FoxOs with beta-catenin, beta-catenin is required for the stimulation of FoxO target genes by H(2)O(2), and H(2)O(2) promotes FoxO-mediated transcription at the expense of Wnt-/T-cell factor-mediated transcription and osteoblast differentiation. Furthermore, beta-catenin overexpression is sufficient to prevent FoxO-mediated suppression of T-cell factor transcription. These results demonstrate that diversion of the limited pool of beta-catenin from T-cell factor- to FoxO-mediated transcription in osteoblastic cells may account, at least in part, for the attenuation of osteoblastogenesis and bone formation by the age-dependent increase in oxidative stress.
              Article 0 comments Cited 159 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: MDPI
                ISSN (Electronic): 1422-0067
                Publication date (Electronic): 12 October 2017
                Publication date Collection: October 2017
                Volume: 18
                Issue: 10
                Electronic Location Identifier: 2132
                Affiliations
                Key Laboratory for Space Bioscience and Biotechnology, Bone Metabolism Lab, School of Life Sciences, Northwestern Polytechnical University, Xi’an 710072, China; tianye@ 123456nwpu.edu.cn (Y.T.); xiaoli225@ 123456mail.nwpu.edu.cn (X.M.); chaofei-yang2015@ 123456mail.nwpu.edu.cn (C.Y.); suph@ 123456mail.nwpu.edu.cn (P.S.); yinchong42@ 123456mail.nwpu.edu.cn (C.Y.)
                Author notes
                [* ]Correspondence: qianair@ 123456nwpu.edu.cn
                Author information
                https://orcid.org/0000-0002-0740-9218
                Article
                Publisher ID: ijms-18-02132
                DOI: 10.3390/ijms18102132
                PMC ID: 5666814
                PubMed ID: 29023398
                SO-VID: c12037fb-0552-4b43-bf02-04b7379dcac3
                Copyright © © 2017 by the authors.
                License:

                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
                Date received : 31 August 2017
                Date accepted : 09 October 2017
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: oxidative stress,bone loss,microgravity,radiation,countermeasure
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: oxidative stress, bone loss, microgravity, radiation, countermeasure

                Comments

                Comment on this article

                scite_

                Similar content81

                See all similar

                Cited by26

                See all cited by

                Most referenced authors1,271

                See all reference authors