For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
20
views
71
references
 Top references
cited by
144
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      475
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: not found

      ROS and diseases: role in metabolism and energy supply

      review-article
      Author(s): ,
      Publication date (Electronic):
      Journal: Molecular and Cellular Biochemistry
      Publisher: Springer US
      Keywords: ROS, Pathology, Diseases, Metabolism, Homeostasis

      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

          Researches dedicated to reactive oxygen species (ROS) had been performed for decades, yet the outcomes remain controversial. With the relentless effort of studies, researchers have explored the role of ROS in biosystem and various diseases. ROS are beneficial for biosystem presenting as signalling molecules and enhancing immunologic defence. However, they also have harmful effects such as causing tissue and organ damages. The results are controversial in studies focusing on ROS and ROS-related diseases by regulating ROS with inhibitors or promotors. These competing results hindered the process for further investigation of the specific mechanisms lying behind. The opinions presented in this review interpret the researches of ROS from a different dimension that might explain the competing results of ROS introduced so far from a broader perspective. This review brings a different thinking to researchers, with the neglected features and potentials of ROS, to relate their works with ROS and to explore the mechanisms between their subject and ROS.

          Related collections

          Most cited references71

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

          NLRP3 inflammasome activation: The convergence of multiple signalling pathways on ROS production?

          Jurg Tschopp, Kate Schroder (2010)
          The NLR family, pyrin domain-containing 3 (NLRP3) inflammasome is a multiprotein complex that activates caspase 1, leading to the processing and secretion of the pro-inflammatory cytokines interleukin-1beta (IL-1beta) and IL-18. The NLRP3 inflammasome is activated by a wide range of danger signals that derive not only from microorganisms but also from metabolic dysregulation. It is unclear how these highly varied stress signals can be detected by a single inflammasome. In this Opinion article, we review the different signalling pathways that have been proposed to engage the NLRP3 inflammasome and suggest a model in which one of the crucial elements for NLRP3 activation is the generation of reactive oxygen species (ROS).
          Article 0 comments Cited 626 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            TLR signaling augments macrophage bactericidal activity through mitochondrial ROS

            A. West, Igor E. Brodsky, Christoph Rahner … (2011)
            Reactive oxygen species (ROS) are essential components of the innate immune response against intracellular bacteria, and it is thought that professional phagocytes generate ROS primarily via the phagosomal NADPH oxidase (Phox) machinery 1 . However, recent studies have suggested that mitochondrial ROS (mROS) also contribute to macrophage bactericidal activity, although the mechanisms linking innate immune signaling to mitochondria for mROS generation remain unclear 2-4 . Here we demonstrate that engagement of a subset of Toll-like receptors (TLR1, TLR2 and TLR4) results in the recruitment of mitochondria to macrophage phagosomes and augments mROS production. This response involves translocation of the TLR signaling adapter tumor necrosis factor receptor-associated factor 6 (TRAF6) to mitochondria where it engages evolutionarily conserved signaling intermediate in Toll pathways (ECSIT), a protein implicated in mitochondrial respiratory chain assembly 5 . Interaction with TRAF6 leads to ECSIT ubiquitination and enrichment at the mitochondrial periphery, resulting in increased mitochondrial and cellular ROS generation. ECSIT and TRAF6 depleted macrophages exhibit decreased levels of TLR-induced ROS and are significantly impaired in their ability to kill intracellular bacteria. Additionally, reducing macrophage mROS by expressing catalase in mitochondria results in defective bacterial killing, confirming the role of mROS in bactericidal activity. These results therefore reveal a novel pathway linking innate immune signaling to mitochondria, implicate mROS as important components of antibacterial responses, and further establish mitochondria as hubs for innate immune signaling.
            Article 0 comments Cited 591 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Reactive oxygen species promote TNFalpha-induced death and sustained JNK activation by inhibiting MAP kinase phosphatases.

              Hideaki Kamata, Shi-Ichi Honda, Shin Maeda … (2005)
              TNFalpha is a pleiotropic cytokine that induces either cell proliferation or cell death. Inhibition of NF-kappaB activation increases susceptibility to TNFalpha-induced death, concurrent with sustained JNK activation, an important contributor to the death response. Sustained JNK activation in NF-kappaB-deficient cells was suggested to depend on reactive oxygen species (ROS), but how ROS affect JNK activation was unclear. We now show that TNFalpha-induced ROS, whose accumulation is suppressed by mitochondrial superoxide dismutase, cause oxidation and inhibition of JNK-inactivating phosphatases by converting their catalytic cysteine to sulfenic acid. This results in sustained JNK activation, which is required for cytochrome c release and caspase 3 cleavage, as well as necrotic cell death. Treatment of cells or experimental animals with an antioxidant prevents H(2)O(2) accumulation, JNK phosphatase oxidation, sustained JNK activity, and both forms of cell death. Antioxidant treatment also prevents TNFalpha-mediated fulminant liver failure without affecting liver regeneration.
              Article 0 comments Cited 432 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Shenshu Yang:
                ORCID: http://orcid.org/0000-0002-3641-3312
                517691576@qq.com
                Gaojian Lian: 714237626@qq.com
                Journal
                Journal ID (nlm-ta): Mol Cell Biochem
                Journal ID (iso-abbrev): Mol. Cell. Biochem
                Title: Molecular and Cellular Biochemistry
                Publisher: Springer US (New York )
                ISSN (Print): 0300-8177
                ISSN (Electronic): 1573-4919
                Publication date (Electronic): 7 December 2019
                Publication date (Print): 2020
                Volume: 467
                Issue: 1
                Pages: 1-12
                Affiliations
                GRID grid.412017.1, ISNI 0000 0001 0266 8918, Hengyang Medical School, , University of South China, ; Hengyang City, Hunan Province 421001 China
                Author information
                http://orcid.org/0000-0002-3641-3312
                Article
                Publisher ID: 3667
                DOI: 10.1007/s11010-019-03667-9
                PMC ID: 7089381
                PubMed ID: 31813106
                SO-VID: c3e2edca-7a2d-40ca-835f-1d33ea2c4f3b
                Copyright © © Springer Science+Business Media, LLC, part of Springer Nature 2019
                License:

                This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

                History
                Date received : 14 July 2019
                Date accepted : 30 November 2019
                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © Springer Science+Business Media, LLC, part of Springer Nature 2020

                ScienceOpen disciplines: Biochemistry
                Keywords: ros,pathology,diseases,metabolism,homeostasis
                Data availability:
                ScienceOpen disciplines: Biochemistry
                Keywords: ros, pathology, diseases, metabolism, homeostasis

                Comments

                Comment on this article

                scite_

                Similar content475

                See all similar

                Cited by141

                See all cited by

                Most referenced authors1,823

                See all reference authors