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      S-glutathionylation, friend or foe in cardiovascular health and disease

      review-article
      Author(s): 1 , 1 , ∗
      Publication date (Electronic):
      Journal: Redox Biology
      Publisher: Elsevier
      Keywords: Cardiovascular disease, Glutathione, S-glutathionylation

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          Abstract

          Glutathione is a low molecular weight thiol that is present at high levels in the cell. The high levels of glutathione in the cell make it one of the most abundant antioxidants contributing to cellular redox homeostasis. As a general rule, throughout cardiovascular disease and progression there is an imbalance in redox homeostasis characterized by reactive oxygen species overproduction and glutathione underproduction. As research into these imbalances continues, glutathione concentrations are increasingly being observed to drive various physiological and pathological signaling responses. Interestingly in addition to acting directly as an antioxidant, glutathione is capable of post translational modifications (S-glutathionylation) of proteins through both chemical interactions and enzyme mediated events. This review will discuss both the chemical and enzyme-based S-glutathionylation of proteins involved in cardiovascular pathologies and angiogenesis.

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          VEGF in Signaling and Disease: Beyond Discovery and Development

          Rajendra Apte, Daniel S. Chen, Napoleone Ferrara (2019)
          The discovery of vascular endothelial-derived growth factor (VEGF) has revolutionized our understanding of vasculogenesis and angiogenesis during development and physiological homeostasis. Over a short span of two decades, our understanding of the molecular mechanisms by which VEGF coordinates neurovascular homeostasis has become more sophisticated. The central role of VEGF in the pathogenesis of diverse cancers and blinding eye diseases has also become evident. Elucidation of the molecular regulation of VEGF and the transformative development of multiple therapeutic pathways targeting VEGF directly or indirectly is a powerful case study of how fundamental research can guide innovation and translation. It is also an elegant example of how agnostic discovery and can transform our understanding of human disease. This review will highlight critical nodal points in VEGF biology including recent developments in immunotherapy for cancer and multi-target approaches in neovascular eye disease.
          Article 0 comments Cited 741 times – based on 0 reviews     Review now
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            The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis.

            Sumanth D. Prabhu, Nikolaos G. Frangogiannis (2016)
            In adult mammals, massive sudden loss of cardiomyocytes after infarction overwhelms the limited regenerative capacity of the myocardium, resulting in the formation of a collagen-based scar. Necrotic cells release danger signals, activating innate immune pathways and triggering an intense inflammatory response. Stimulation of toll-like receptor signaling and complement activation induces expression of proinflammatory cytokines (such as interleukin-1 and tumor necrosis factor-α) and chemokines (such as monocyte chemoattractant protein-1/ chemokine (C-C motif) ligand 2 [CCL2]). Inflammatory signals promote adhesive interactions between leukocytes and endothelial cells, leading to extravasation of neutrophils and monocytes. As infiltrating leukocytes clear the infarct from dead cells, mediators repressing inflammation are released, and anti-inflammatory mononuclear cell subsets predominate. Suppression of the inflammatory response is associated with activation of reparative cells. Fibroblasts proliferate, undergo myofibroblast transdifferentiation, and deposit large amounts of extracellular matrix proteins maintaining the structural integrity of the infarcted ventricle. The renin-angiotensin-aldosterone system and members of the transforming growth factor-β family play an important role in activation of infarct myofibroblasts. Maturation of the scar follows, as a network of cross-linked collagenous matrix is formed and granulation tissue cells become apoptotic. This review discusses the cellular effectors and molecular signals regulating the inflammatory and reparative response after myocardial infarction. Dysregulation of immune pathways, impaired suppression of postinfarction inflammation, perturbed spatial containment of the inflammatory response, and overactive fibrosis may cause adverse remodeling in patients with infarction contributing to the pathogenesis of heart failure. Therapeutic modulation of the inflammatory and reparative response may hold promise for the prevention of postinfarction heart failure.
            Article 0 comments Cited 529 times – based on 0 reviews     Review now
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              Redox environment of the cell as viewed through the redox state of the glutathione disulfide/glutathione couple.

              F Q Schafer, G R Buettner (2001)
              Redox state is a term used widely in the research field of free radicals and oxidative stress. Unfortunately, it is used as a general term referring to relative changes that are not well defined or quantitated. In this review we provide a definition for the redox environment of biological fluids, cell organelles, cells, or tissue. We illustrate how the reduction potential of various redox couples can be estimated with the Nernst equation and show how pH and the concentrations of the species comprising different redox couples influence the reduction potential. We discuss how the redox state of the glutathione disulfide-glutathione couple (GSSG/2GSH) can serve as an important indicator of redox environment. There are many redox couples in a cell that work together to maintain the redox environment; the GSSG/2GSH couple is the most abundant redox couple in a cell. Changes of the half-cell reduction potential (E(hc)) of the GSSG/2GSH couple appear to correlate with the biological status of the cell: proliferation E(hc) approximately -240 mV; differentiation E(hc) approximately -200 mV; or apoptosis E(hc) approximately -170 mV. These estimates can be used to more fully understand the redox biochemistry that results from oxidative stress. These are the first steps toward a new quantitative biology, which hopefully will provide a rationale and understanding of the cellular mechanisms associated with cell growth and development, signaling, and reductive or oxidative stress.
              Article 0 comments Cited 512 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                C.B. Pattillo
                Journal
                Journal ID (nlm-ta): Redox Biol
                Journal ID (iso-abbrev): Redox Biol
                Title: Redox Biology
                Publisher: Elsevier
                ISSN (Electronic): 2213-2317
                Publication date PMC-release: 22 August 2020
                Publication date Collection: October 2020
                Publication date (Electronic): 22 August 2020
                Volume: 37
                Electronic Location Identifier: 101693
                Affiliations
                [1]Department of Cellular and Molecular Physiology, Louisiana State Health Science Center, Shreveport, LA, USA
                Author notes
                [∗ ]Corresponding author. cpatt7@ 123456lsuhsc.edu
                [1]

                Both authors contributed equally.

                Article
                Publisher Item ID: S2213-2317(20)30898-3 Publisher ID: 101693
                DOI: 10.1016/j.redox.2020.101693
                PMC ID: 7767732
                PubMed ID: 32912836
                SO-VID: 56beefb9-856d-4a8b-8154-863b7019b820
                Copyright © © 2020 Published by Elsevier B.V.
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 1 April 2020
                Date revision received : 12 August 2020
                Date accepted : 16 August 2020
                Categories
                Subject: Review Article

                Keywords: cardiovascular disease,glutathione,s-glutathionylation
                Data availability:
                Keywords: cardiovascular disease, glutathione, s-glutathionylation

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