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      Oxidative Stress in COPD

      editorial

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          Abstract

          Numerous studies over the years have shown that oxidative stress plays a major role in the development of the disease. Oxidative stress involvement in COPD opens up the possibility of using antioxidant therapies in the treatment of the disease. However, so far, these therapies have shown no clinical benefit indicating that more basic research efforts are needed to understand the underlying mechanisms by which oxidative stress leads to the development of COPD.

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          Oxidative stress in COPD.

          Paul Kirkham, Peter Barnes (2013)
          Oxidative stress is now recognized as a major predisposing factor in the pathogenesis of COPD. Existing therapies for COPD are ineffective at halting disease progression, with bronchodilators being the mainstay of pharmacotherapy, providing symptomatic relief only. It is, therefore, important for a better understanding of the underlying mechanisms by which oxidative stress drives disease pathogenesis to develop novel and more effective therapies. Antioxidant capacity in COPD is substantially reduced as a result of cigarette smoking and exacerbations, with oxidative stress persisting long after the cessation of cigarette smoking or exacerbation, due to the continued production of reactive oxygen species from endogenous sources. We discuss (1) how oxidative stress arises in the lung, (2) how it is neutralized, (3) what genetic factors may predispose to the development of COPD, and (4) how this impacts inflammation and autoimmunity in the development of emphysema and small airways disease. Finally, various strategies have been considered to neutralize the increased oxidative burden present in COPD. This review highlights why current antioxidant strategies have so far failed and what promising alternatives are on the horizon. Moreover, a number of studies have shown that there is no single "magic bullet" to combat oxidative stress, but instead a combination therapy, targeting oxidative stress in the various subcellular compartments, may prove to be more effective in COPD.
          Article 0 comments Cited 263 times – based on 0 reviews     Review now
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            Chronic bronchitis and chronic obstructive pulmonary disease.

            Victor Kim, Gerard J. Criner (2013)
            Chronic bronchitis (CB) is a common but variable phenomenon in chronic obstructive pulmonary disease (COPD). It has numerous clinical consequences, including an accelerated decline in lung function, greater risk of the development of airflow obstruction in smokers, a predisposition to lower respiratory tract infection, higher exacerbation frequency, and worse overall mortality. CB is caused by overproduction and hypersecretion of mucus by goblet cells, which leads to worsening airflow obstruction by luminal obstruction of small airways, epithelial remodeling, and alteration of airway surface tension predisposing to collapse. Despite its clinical sequelae, little is known about the pathophysiology of CB and goblet cell hyperplasia in COPD, and treatment options are limited. In addition, it is becoming increasingly apparent that in the classic COPD spectrum, with emphysema on one end and CB on the other, most patients lie somewhere in the middle. It is known now that many patients with severe emphysema can develop CB, and small airway pathology has been linked to worse clinical outcomes, such as increased mortality and lesser improvement in lung function after lung volume reduction surgery. However, in recent years, a greater understanding of the importance of CB as a phenotype to identify patients with a beneficial response to therapy has been described. Herein we review the epidemiology of CB, the evidence behind its clinical consequences, the current understanding of the pathophysiology of goblet cell hyperplasia in COPD, and current therapies for CB.
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              Role of Nrf2 and Its Activators in Respiratory Diseases

              Qinmei Liu, Yun. Gao, Xinxin Ci (2019)
              Transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) is a major regulator of antioxidant response element- (ARE-) driven cytoprotective protein expression. The activation of Nrf2 signaling plays an essential role in preventing cells and tissues from injury induced by oxidative stress. Under the unstressed conditions, natural inhibitor of Nrf2, Kelch-like ECH-associated protein 1 (Keap1), traps Nrf2 in the cytoplasm and promotes the degradation of Nrf2 by the 26S proteasome. Nevertheless, stresses including highly oxidative microenvironments, impair the ability of Keap1 to target Nrf2 for ubiquitination and degradation, and induce newly synthesized Nrf2 to translocate to the nucleus to bind with ARE. Due to constant exposure to external environments, including diverse pollutants and other oxidants, the redox balance maintained by Nrf2 is fairly important to the airways. To date, researchers have discovered that Nrf2 deletion results in high susceptibility and severity of insults in various models of respiratory diseases, including bronchopulmonary dysplasia (BPD), respiratory infections, acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD), asthma, idiopathic pulmonary fibrosis (IPF), and lung cancer. Conversely, Nrf2 activation confers protective effects on these lung disorders. In the present review, we summarize Nrf2 involvement in the pathogenesis of the above respiratory diseases that have been identified by experimental models and human studies and describe the protective effects of Nrf2 inducers on these diseases.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Clin Med
                Journal ID (iso-abbrev): J Clin Med
                Journal ID (publisher-id): jcm
                Title: Journal of Clinical Medicine
                Publisher: MDPI
                ISSN (Electronic): 2077-0383
                Publication date (Electronic): 13 November 2019
                Publication date Collection: November 2019
                Volume: 8
                Issue: 11
                Electronic Location Identifier: 1953
                Affiliations
                [1 ]Instituto de Investigación Sanitaria INCLIVA, Fundación Investigación Hospital Clínico Universitario Valencia, Avda. Menéndez y Pelayo, 4, 46010 Valencia, Spain; mariamagallon94@ 123456gmail.com (M.M.); mer_navarro2002@ 123456yahoo.es (M.M.N.-G.)
                [2 ]Rare Respiratory Diseases Group, Department of Physiology, School of Medicine, University of Valencia, Avda. Blasco Ibáñez, 17, 46010 Valencia, Spain
                Author notes
                [* ]Correspondence: Francisco.Dasi@ 123456uv.es ; Tel.: +34-676-515-598
                Author information
                https://orcid.org/0000-0002-6020-7172
                https://orcid.org/0000-0003-2938-2965
                Article
                Publisher ID: jcm-08-01953
                DOI: 10.3390/jcm8111953
                PMC ID: 6912514
                PubMed ID: 31766150
                SO-VID: 5b4c93a6-8507-4a0d-8031-2104345acc92
                Copyright © © 2019 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 : 30 October 2019
                Date accepted : 06 November 2019
                Categories
                Subject: Editorial

                Keywords: oxidative stress,copd,alpha-1 antitrypsin deficiency,antioxidants
                Data availability:
                Keywords: oxidative stress, copd, alpha-1 antitrypsin deficiency, antioxidants

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