Antioxidants & bronchopulmonary dysplasia: Beating the system or beating a dead horse?
Preterm birth is a primary cause of worldwide childhood mortality. Bronchopulmonary dysplasia, characterized by impaired alveolar and lung vascular development, affects 25–50% of extremely low birth weight (BW;
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| Veröffentlicht in: | Free radical biology & medicine 2019-10, Vol.142, p.138-145 |
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| creator | Ofman, Gaston Tipple, Trent E. |
| description | Preterm birth is a primary cause of worldwide childhood mortality. Bronchopulmonary dysplasia, characterized by impaired alveolar and lung vascular development, affects 25–50% of extremely low birth weight (BW; |
| doi_str_mv | 10.1016/j.freeradbiomed.2019.01.038 |
| format | Article |
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Reactive oxygen intermediates play a key role in the development of lung disease but, despite promising preclinical therapies, antioxidants have failed to translate into meaningful clinical interventions to decrease the incidence of lung disease in premature infants. In this review we will summarize the state of the art research developments in regards to antioxidants and premature lung disease and discuss the limitations of antioxidant therapies in order to more fully comprehend the reasons why therapeutic antioxidant administration failed to prevent BPD. Finally we will review promising therapeutic strategies and targets.
[Display omitted]
•Antioxidant therapies have failed to decrease the incidence of bronchopulmonary dysplasia.•Redox signaling is part of normal development of fetal and neonatal lung as well as in lung disease.•Timing, specificity, bioavailability and personalized medicine must be considered for future therapeutic trials to succeed.</description><identifier>ISSN: 0891-5849</identifier><identifier>EISSN: 1873-4596</identifier><identifier>DOI: 10.1016/j.freeradbiomed.2019.01.038</identifier><identifier>PMID: 30769161</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Antioxidants - therapeutic use ; Bronchopulmonary Dysplasia - genetics ; Bronchopulmonary Dysplasia - metabolism ; Bronchopulmonary Dysplasia - physiopathology ; Bronchopulmonary Dysplasia - therapy ; Child ; Dietary Supplements ; Glutathione - administration & dosage ; Glutathione - metabolism ; Humans ; Infant, Newborn ; Infant, Premature ; Infant, Very Low Birth Weight ; Intensive Care Units, Neonatal ; Lung - drug effects ; Lung - metabolism ; Lung - physiopathology ; NF-E2-Related Factor 2 - agonists ; NF-E2-Related Factor 2 - genetics ; NF-E2-Related Factor 2 - metabolism ; Oxidative Stress - drug effects ; Precision Medicine - methods ; Reactive Oxygen Species - antagonists & inhibitors ; Reactive Oxygen Species - metabolism ; Selenium - administration & dosage ; Selenium - metabolism ; Thioredoxins - agonists ; Thioredoxins - genetics ; Thioredoxins - metabolism</subject><ispartof>Free radical biology & medicine, 2019-10, Vol.142, p.138-145</ispartof><rights>2019 Elsevier Inc.</rights><rights>Copyright © 2019 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c383t-c6b1bcf5280b9231d1be7154743b4932b196643c0e60be6d561a45bc62fa818b3</citedby><cites>FETCH-LOGICAL-c383t-c6b1bcf5280b9231d1be7154743b4932b196643c0e60be6d561a45bc62fa818b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0891584918325486$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30769161$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ofman, Gaston</creatorcontrib><creatorcontrib>Tipple, Trent E.</creatorcontrib><title>Antioxidants & bronchopulmonary dysplasia: Beating the system or beating a dead horse?</title><title>Free radical biology & medicine</title><addtitle>Free Radic Biol Med</addtitle><description>Preterm birth is a primary cause of worldwide childhood mortality. Bronchopulmonary dysplasia, characterized by impaired alveolar and lung vascular development, affects 25–50% of extremely low birth weight (BW; <1 kg) infants. Abnormalities in lung function persist into childhood in affected infants and are second only to asthma in terms of childhood respiratory disease healthcare costs. While advances in the medical care of preterm infants have reduced mortality, the incidence of BPD has not decreased in the past 10 years.
Reactive oxygen intermediates play a key role in the development of lung disease but, despite promising preclinical therapies, antioxidants have failed to translate into meaningful clinical interventions to decrease the incidence of lung disease in premature infants. In this review we will summarize the state of the art research developments in regards to antioxidants and premature lung disease and discuss the limitations of antioxidant therapies in order to more fully comprehend the reasons why therapeutic antioxidant administration failed to prevent BPD. Finally we will review promising therapeutic strategies and targets.
[Display omitted]
•Antioxidant therapies have failed to decrease the incidence of bronchopulmonary dysplasia.•Redox signaling is part of normal development of fetal and neonatal lung as well as in lung disease.•Timing, specificity, bioavailability and personalized medicine must be considered for future therapeutic trials to succeed.</description><subject>Antioxidants - therapeutic use</subject><subject>Bronchopulmonary Dysplasia - genetics</subject><subject>Bronchopulmonary Dysplasia - metabolism</subject><subject>Bronchopulmonary Dysplasia - physiopathology</subject><subject>Bronchopulmonary Dysplasia - therapy</subject><subject>Child</subject><subject>Dietary Supplements</subject><subject>Glutathione - administration & dosage</subject><subject>Glutathione - metabolism</subject><subject>Humans</subject><subject>Infant, Newborn</subject><subject>Infant, Premature</subject><subject>Infant, Very Low Birth Weight</subject><subject>Intensive Care Units, Neonatal</subject><subject>Lung - drug effects</subject><subject>Lung - metabolism</subject><subject>Lung - physiopathology</subject><subject>NF-E2-Related Factor 2 - agonists</subject><subject>NF-E2-Related Factor 2 - genetics</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Oxidative Stress - drug effects</subject><subject>Precision Medicine - methods</subject><subject>Reactive Oxygen Species - antagonists & inhibitors</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Selenium - administration & dosage</subject><subject>Selenium - metabolism</subject><subject>Thioredoxins - agonists</subject><subject>Thioredoxins - genetics</subject><subject>Thioredoxins - metabolism</subject><issn>0891-5849</issn><issn>1873-4596</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkE9vEzEQxS1URNPCV0CWKiEuu3jWXscuhypULSBV4gJcLf-ZJY5218HeIPLt2SjJgVtPI828N0_vR8gNsBoYyA-busuI2QYX04ChbhjomkHNuHpBFqCWvBKtlhdkwZSGqlVCX5KrUjaMMdFy9YpccraUGiQsyM_VOMX0NwY7ToW-oy6n0a_TdtcPabR5T8O-bHtbor2ln9BOcfxFpzXSsi8TDjRl6k5bSwPaQNcpF7x7TV52ti_45jSvyY_Hh-_3X6qnb5-_3q-eKs8VnyovHTjftY1iTjccAjhcQiuWgjuheeNASym4ZyiZQxlaCVa0zsumswqU49fk_fHvNqffOyyTGWLx2Pd2xLQrpgElQSipxSz9eJT6nErJ2JltjsNc0QAzB7BmY_4Daw5gDQMzg53db09BO3e4nb1nkrPg4SjAue6fiNkUH3H0GGJGP5mQ4rOC_gHd05Fn</recordid><startdate>201910</startdate><enddate>201910</enddate><creator>Ofman, Gaston</creator><creator>Tipple, Trent E.</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>201910</creationdate><title>Antioxidants & bronchopulmonary dysplasia: Beating the system or beating a dead horse?</title><author>Ofman, Gaston ; Tipple, Trent E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c383t-c6b1bcf5280b9231d1be7154743b4932b196643c0e60be6d561a45bc62fa818b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Antioxidants - therapeutic use</topic><topic>Bronchopulmonary Dysplasia - genetics</topic><topic>Bronchopulmonary Dysplasia - metabolism</topic><topic>Bronchopulmonary Dysplasia - physiopathology</topic><topic>Bronchopulmonary Dysplasia - therapy</topic><topic>Child</topic><topic>Dietary Supplements</topic><topic>Glutathione - administration & dosage</topic><topic>Glutathione - metabolism</topic><topic>Humans</topic><topic>Infant, Newborn</topic><topic>Infant, Premature</topic><topic>Infant, Very Low Birth Weight</topic><topic>Intensive Care Units, Neonatal</topic><topic>Lung - drug effects</topic><topic>Lung - metabolism</topic><topic>Lung - physiopathology</topic><topic>NF-E2-Related Factor 2 - agonists</topic><topic>NF-E2-Related Factor 2 - genetics</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>Oxidative Stress - drug effects</topic><topic>Precision Medicine - methods</topic><topic>Reactive Oxygen Species - antagonists & inhibitors</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Selenium - administration & dosage</topic><topic>Selenium - metabolism</topic><topic>Thioredoxins - agonists</topic><topic>Thioredoxins - genetics</topic><topic>Thioredoxins - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ofman, Gaston</creatorcontrib><creatorcontrib>Tipple, Trent E.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Free radical biology & medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ofman, Gaston</au><au>Tipple, Trent E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antioxidants & bronchopulmonary dysplasia: Beating the system or beating a dead horse?</atitle><jtitle>Free radical biology & medicine</jtitle><addtitle>Free Radic Biol Med</addtitle><date>2019-10</date><risdate>2019</risdate><volume>142</volume><spage>138</spage><epage>145</epage><pages>138-145</pages><issn>0891-5849</issn><eissn>1873-4596</eissn><abstract>Preterm birth is a primary cause of worldwide childhood mortality. Bronchopulmonary dysplasia, characterized by impaired alveolar and lung vascular development, affects 25–50% of extremely low birth weight (BW; <1 kg) infants. Abnormalities in lung function persist into childhood in affected infants and are second only to asthma in terms of childhood respiratory disease healthcare costs. While advances in the medical care of preterm infants have reduced mortality, the incidence of BPD has not decreased in the past 10 years.
Reactive oxygen intermediates play a key role in the development of lung disease but, despite promising preclinical therapies, antioxidants have failed to translate into meaningful clinical interventions to decrease the incidence of lung disease in premature infants. In this review we will summarize the state of the art research developments in regards to antioxidants and premature lung disease and discuss the limitations of antioxidant therapies in order to more fully comprehend the reasons why therapeutic antioxidant administration failed to prevent BPD. Finally we will review promising therapeutic strategies and targets.
[Display omitted]
•Antioxidant therapies have failed to decrease the incidence of bronchopulmonary dysplasia.•Redox signaling is part of normal development of fetal and neonatal lung as well as in lung disease.•Timing, specificity, bioavailability and personalized medicine must be considered for future therapeutic trials to succeed.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>30769161</pmid><doi>10.1016/j.freeradbiomed.2019.01.038</doi><tpages>8</tpages></addata></record> |
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| subjects | Antioxidants - therapeutic use Bronchopulmonary Dysplasia - genetics Bronchopulmonary Dysplasia - metabolism Bronchopulmonary Dysplasia - physiopathology Bronchopulmonary Dysplasia - therapy Child Dietary Supplements Glutathione - administration & dosage Glutathione - metabolism Humans Infant, Newborn Infant, Premature Infant, Very Low Birth Weight Intensive Care Units, Neonatal Lung - drug effects Lung - metabolism Lung - physiopathology NF-E2-Related Factor 2 - agonists NF-E2-Related Factor 2 - genetics NF-E2-Related Factor 2 - metabolism Oxidative Stress - drug effects Precision Medicine - methods Reactive Oxygen Species - antagonists & inhibitors Reactive Oxygen Species - metabolism Selenium - administration & dosage Selenium - metabolism Thioredoxins - agonists Thioredoxins - genetics Thioredoxins - metabolism |
| title | Antioxidants & bronchopulmonary dysplasia: Beating the system or beating a dead horse? |
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