For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
15
views
291
references
 Top references
cited by
53
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      659
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Role of Oxidative Stress in Reperfusion following Myocardial Ischemia and Its Treatments

      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

          Myocardial ischemia is a disease with high morbidity and mortality, for which reperfusion is currently the standard intervention. However, the reperfusion may lead to further myocardial damage, known as myocardial ischemia/reperfusion injury (MI/RI). Oxidative stress is one of the most important pathological mechanisms in reperfusion injury, which causes apoptosis, autophagy, inflammation, and some other damage in cardiomyocytes through multiple pathways, thus causing irreversible cardiomyocyte damage and cardiac dysfunction. This article reviews the pathological mechanisms of oxidative stress involved in reperfusion injury and the interventions for different pathways and targets, so as to form systematic treatments for oxidative stress-induced myocardial reperfusion injury and make up for the lack of monotherapy.

          Related collections

          Most cited references291

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

          The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology.

          Karen Bedard, Karl-Heinz Krause (2007)
          For a long time, superoxide generation by an NADPH oxidase was considered as an oddity only found in professional phagocytes. Over the last years, six homologs of the cytochrome subunit of the phagocyte NADPH oxidase were found: NOX1, NOX3, NOX4, NOX5, DUOX1, and DUOX2. Together with the phagocyte NADPH oxidase itself (NOX2/gp91(phox)), the homologs are now referred to as the NOX family of NADPH oxidases. These enzymes share the capacity to transport electrons across the plasma membrane and to generate superoxide and other downstream reactive oxygen species (ROS). Activation mechanisms and tissue distribution of the different members of the family are markedly different. The physiological functions of NOX family enzymes include host defense, posttranlational processing of proteins, cellular signaling, regulation of gene expression, and cell differentiation. NOX enzymes also contribute to a wide range of pathological processes. NOX deficiency may lead to immunosuppresion, lack of otoconogenesis, or hypothyroidism. Increased NOX activity also contributes to a large number or pathologies, in particular cardiovascular diseases and neurodegeneration. This review summarizes the current state of knowledge of the functions of NOX enzymes in physiology and pathology.
          Article 0 comments Cited 826 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Endoplasmic reticulum stress: cell life and death decisions.

            C. Xu (2005)
            Disturbances in the normal functions of the ER lead to an evolutionarily conserved cell stress response, the unfolded protein response, which is aimed initially at compensating for damage but can eventually trigger cell death if ER dysfunction is severe or prolonged. The mechanisms by which ER stress leads to cell death remain enigmatic, with multiple potential participants described but little clarity about which specific death effectors dominate in particular cellular contexts. Important roles for ER-initiated cell death pathways have been recognized for several diseases, including hypoxia, ischemia/reperfusion injury, neurodegeneration, heart disease, and diabetes.
            Article 0 comments Cited 635 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: found

              Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS

              Edward T Chouchani, Victoria R Pell, Edoardo Gaude … (2015)
              Ischaemia-reperfusion (IR) injury occurs when blood supply to an organ is disrupted and then restored, and underlies many disorders, notably heart attack and stroke. While reperfusion of ischaemic tissue is essential for survival, it also initiates oxidative damage, cell death, and aberrant immune responses through generation of mitochondrial reactive oxygen species (ROS) 1-5 . Although mitochondrial ROS production in IR is established, it has generally been considered a non-specific response to reperfusion 1,3 . Here, we developed a comparative in vivo metabolomic analysis and unexpectedly identified widely conserved metabolic pathways responsible for mitochondrial ROS production during IR. We showed that selective accumulation of the citric acid cycle (CAC) intermediate succinate is a universal metabolic signature of ischaemia in a range of tissues and is responsible for mitochondrial ROS production during reperfusion. Ischaemic succinate accumulation arises from reversal of succinate dehydrogenase (SDH), which in turn is driven by fumarate overflow from purine nucleotide breakdown and partial reversal of the malate/aspartate shuttle. Upon reperfusion, the accumulated succinate is rapidly re-oxidised by SDH, driving extensive ROS generation by reverse electron transport (RET) at mitochondrial complex I. Decreasing ischaemic succinate accumulation by pharmacological inhibition is sufficient to ameliorate in vivo IR injury in murine models of heart attack and stroke. Thus, we have identified a conserved metabolic response of tissues to ischaemia and reperfusion that unifies many hitherto unconnected aspects of IR injury. Furthermore, these findings reveal a novel pathway for metabolic control of ROS production in vivo, while demonstrating that inhibition of ischaemic succinate accumulation and its oxidation upon subsequent reperfusion is a potential therapeutic target to decrease IR injury in a range of pathologies.
              Article 0 comments Cited 611 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Mingjing Zhao:
                ORCID: https://orcid.org/0000-0003-2738-7500
                Xiangning Cui:
                ORCID: https://orcid.org/0000-0002-4745-2384
                Journal
                Journal ID (nlm-ta): Oxid Med Cell Longev
                Journal ID (iso-abbrev): Oxid Med Cell Longev
                Journal ID (publisher-id): OMCL
                Title: Oxidative Medicine and Cellular Longevity
                Publisher: Hindawi
                ISSN (Print): 1942-0900
                ISSN (Electronic): 1942-0994
                Publication date Collection: 2021
                Publication date (Electronic): 18 May 2021
                Volume: 2021
                Electronic Location Identifier: 6614009
                Affiliations
                1Department of Cardiovascular, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China
                2First Clinical Medical School, Shandong University of Chinese Medicine, Shandong, China
                3Key Laboratory of Chinese Internal Medicine of Ministry of Education, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, China
                Author notes

                Academic Editor: Carlo G. Tocchetti

                Author information
                https://orcid.org/0000-0003-4369-4084
                https://orcid.org/0000-0002-5355-1733
                https://orcid.org/0000-0003-3550-0729
                https://orcid.org/0000-0002-6135-0915
                https://orcid.org/0000-0001-9673-1905
                https://orcid.org/0000-0001-7881-1231
                https://orcid.org/0000-0003-2738-7500
                https://orcid.org/0000-0002-4745-2384
                Article
                DOI: 10.1155/2021/6614009
                PMC ID: 8149218
                PubMed ID: 34055195
                SO-VID: 2c3c9346-b27b-43ce-92e1-bbf1aa58893c
                Copyright © Copyright © 2021 Mi Xiang et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 30 November 2020
                Date revision received : 21 February 2021
                Date accepted : 29 April 2021
                Funding
                Funded by: National Natural Science Foundation of China
                Award ID: 81973842
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Molecular medicine
                Data availability:
                ScienceOpen disciplines: Molecular medicine

                Comments

                Comment on this article

                scite_

                Similar content659

                See all similar

                Cited by53

                See all cited by

                Most referenced authors3,618

                See all reference authors