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      Redox for Repair: Cold Physical Plasmas and Nrf2 Signaling Promoting Wound Healing

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          Abstract

          Chronic wounds and ulcers are major public health threats. Being a substantial burden for patients and health care systems alike, better understanding of wound pathophysiology and new avenues in the therapy of chronic wounds are urgently needed. Cold physical plasmas are particularly effective in promoting wound closure, irrespective of its etiology. These partially ionized gases deliver a therapeutic cocktail of reactive oxygen and nitrogen species safely at body temperature and without genotoxic side effects. This field of plasma medicine reanimates the idea of redox repair in physiological healing. This review compiles previous findings of plasma effects in wound healing. It discusses new links between plasma treatment of cells and tissues, and the perception and intracellular translation of plasma-derived reactive species via redox signaling pathways. Specifically, (i) molecular switches governing redox-mediated tissue response; (ii) the activation of the nuclear E2-related factor (Nrf2) signaling, together with antioxidative and immunomodulatory responses; and (iii) the stabilization of the scaffolding function and actin network in dermal fibroblasts are emphasized in the light of wound healing.

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          Most cited references109

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          Opposing effects of ERK and JNK-p38 MAP kinases on apoptosis.

          Apoptosis plays an important role during neuronal development, and defects in apoptosis may underlie various neurodegenerative disorders. To characterize molecular mechanisms that regulate neuronal apoptosis, the contributions to cell death of mitogen-activated protein (MAP) kinase family members, including ERK (extracellular signal-regulated kinase), JNK (c-JUN NH2-terminal protein kinase), and p38, were examined after withdrawal of nerve growth factor (NGF) from rat PC-12 pheochromocytoma cells. NGF withdrawal led to sustained activation of the JNK and p38 enzymes and inhibition of ERKs. The effects of dominant-interfering or constitutively activated forms of various components of the JNK-p38 and ERK signaling pathways demonstrated that activation of JNK and p38 and concurrent inhibition of ERK are critical for induction of apoptosis in these cells. Therefore, the dynamic balance between growth factor-activated ERK and stress-activated JNK-p38 pathways may be important in determining whether a cell survives or undergoes apoptosis.
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            The myofibroblast in wound healing and fibrocontractive diseases.

            G Gabbiani (2003)
            The demonstration that fibroblastic cells acquire contractile features during the healing of an open wound, thus modulating into myofibroblasts, has open a new perspective in the understanding of mechanisms leading to wound closure and fibrocontractive diseases. Myofibroblasts synthesize extracellular matrix components such as collagen types I and III and during normal wound healing disappear by apoptosis when epithelialization occurs. The transition from fibroblasts to myofibroblasts is influenced by mechanical stress, TGF-beta and cellular fibronectin (ED-A splice variant). These factors also play important roles in the development of fibrocontractive changes, such as those observed in liver cirrhosis, renal fibrosis, and stroma reaction to epithelial tumours. Copyright 2003 John Wiley & Sons, Ltd.
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              The basic science of wound healing.

              Understanding wound healing today involves much more than simply stating that there are three phases: "inflammation, proliferation, and maturation." Wound healing is a complex series of reactions and interactions among cells and "mediators." Each year, new mediators are discovered and our understanding of inflammatory mediators and cellular interactions grows. This article will attempt to provide a concise report of the current literature on wound healing by first reviewing the phases of wound healing followed by "the players" of wound healing: inflammatory mediators (cytokines, growth factors, proteases, eicosanoids, kinins, and more), nitric oxide, and the cellular elements. The discussion will end with a pictorial essay summarizing the wound-healing process.
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                Author and article information

                Journal
                Antioxidants (Basel)
                Antioxidants (Basel)
                antioxidants
                Antioxidants
                MDPI
                2076-3921
                19 October 2018
                October 2018
                : 7
                : 10
                : 146
                Affiliations
                [1 ]Plasma Life Science, Leibniz Institute for Plasma Science and Technology (INP Greifswald), Felix-Hausdorff-Str. 2, 17489 Greifswald, Germany
                [2 ]ZIK-PRE, Leibniz Institute for Plasma Science and Technology (INP Greifswald), Felix-Hausdorff-Str. 2, 17489 Greifswald, Germany; sander.bekeschus@ 123456inp-greifswald.de
                Author notes
                [* ]Correspondence: anke.schmidt@ 123456inp-greifswald.de ; Tel.: +49-3834-5543958; Fax: +49-3834-554301
                Author information
                https://orcid.org/0000-0001-6488-3904
                https://orcid.org/0000-0002-8773-8862
                Article
                antioxidants-07-00146
                10.3390/antiox7100146
                6210784
                30347767
                3dd0eca4-9bc6-4135-ba1e-71f91ee43c15
                © 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
                : 28 September 2018
                : 18 October 2018
                Categories
                Review

                keap1,kinpen,plasma medicine,reactive oxygen species (ros),reactive nitrogen species (rns),redox regulation

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