When inflammation meets lung development—an update on the pathogenesis of bronchopulmonary dysplasia
Even more than 50 years after its initial description, bronchopulmonary dysplasia (BPD) remains one of the most important and lifelong sequelae following premature birth. Tremendous efforts have been undertaken since then to reduce this ever-increasing disease burden but a therapeutic breakthrough p...
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Published in | Molecular and cellular pediatrics Vol. 9; no. 1; pp. 7 - 12 |
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Main Authors | , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Cham
Springer International Publishing
20.04.2022
Springer Nature B.V SpringerOpen |
Subjects | |
Online Access | Get full text |
ISSN | 2194-7791 2194-7791 |
DOI | 10.1186/s40348-022-00137-z |
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Abstract | Even more than 50 years after its initial description, bronchopulmonary dysplasia (BPD) remains one of the most important and lifelong sequelae following premature birth. Tremendous efforts have been undertaken since then to reduce this ever-increasing disease burden but a therapeutic breakthrough preventing BPD is still not in sight. The inflammatory response provoked in the immature lung is a key driver of distorted lung development and impacts the formation of alveolar, mesenchymal, and vascular structures during a particularly vulnerable time-period. During the last 5 years, new scientific insights have led to an improved pathomechanistic understanding of BPD origins and disease drivers. Within the framework of current scientific progress, concepts involving disruption of the balance of key inflammatory and lung growth promoting pathways by various stimuli, take center stage. Still today, the number of efficient therapeutics available to prevent BPD is limited to a few, well-established pharmacological interventions including postnatal corticosteroids, early caffeine administration, and vitamin A. Recent advances in the clinical care of infants in the neonatal intensive care unit (NICU) have led to improvements in survival without a consistent reduction in the incidence of BPD. Our update provides latest insights from both preclinical models and clinical cohort studies and describes novel approaches to prevent BPD. |
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AbstractList | Even more than 50 years after its initial description, bronchopulmonary dysplasia (BPD) remains one of the most important and lifelong sequelae following premature birth. Tremendous efforts have been undertaken since then to reduce this ever-increasing disease burden but a therapeutic breakthrough preventing BPD is still not in sight. The inflammatory response provoked in the immature lung is a key driver of distorted lung development and impacts the formation of alveolar, mesenchymal, and vascular structures during a particularly vulnerable time-period. During the last 5 years, new scientific insights have led to an improved pathomechanistic understanding of BPD origins and disease drivers. Within the framework of current scientific progress, concepts involving disruption of the balance of key inflammatory and lung growth promoting pathways by various stimuli, take center stage. Still today, the number of efficient therapeutics available to prevent BPD is limited to a few, well-established pharmacological interventions including postnatal corticosteroids, early caffeine administration, and vitamin A. Recent advances in the clinical care of infants in the neonatal intensive care unit (NICU) have led to improvements in survival without a consistent reduction in the incidence of BPD. Our update provides latest insights from both preclinical models and clinical cohort studies and describes novel approaches to prevent BPD. Abstract Even more than 50 years after its initial description, bronchopulmonary dysplasia (BPD) remains one of the most important and lifelong sequelae following premature birth. Tremendous efforts have been undertaken since then to reduce this ever-increasing disease burden but a therapeutic breakthrough preventing BPD is still not in sight. The inflammatory response provoked in the immature lung is a key driver of distorted lung development and impacts the formation of alveolar, mesenchymal, and vascular structures during a particularly vulnerable time-period. During the last 5 years, new scientific insights have led to an improved pathomechanistic understanding of BPD origins and disease drivers. Within the framework of current scientific progress, concepts involving disruption of the balance of key inflammatory and lung growth promoting pathways by various stimuli, take center stage. Still today, the number of efficient therapeutics available to prevent BPD is limited to a few, well-established pharmacological interventions including postnatal corticosteroids, early caffeine administration, and vitamin A. Recent advances in the clinical care of infants in the neonatal intensive care unit (NICU) have led to improvements in survival without a consistent reduction in the incidence of BPD. Our update provides latest insights from both preclinical models and clinical cohort studies and describes novel approaches to prevent BPD. Even more than 50 years after its initial description, bronchopulmonary dysplasia (BPD) remains one of the most important and lifelong sequelae following premature birth. Tremendous efforts have been undertaken since then to reduce this ever-increasing disease burden but a therapeutic breakthrough preventing BPD is still not in sight. The inflammatory response provoked in the immature lung is a key driver of distorted lung development and impacts the formation of alveolar, mesenchymal, and vascular structures during a particularly vulnerable time-period. During the last 5 years, new scientific insights have led to an improved pathomechanistic understanding of BPD origins and disease drivers. Within the framework of current scientific progress, concepts involving disruption of the balance of key inflammatory and lung growth promoting pathways by various stimuli, take center stage. Still today, the number of efficient therapeutics available to prevent BPD is limited to a few, well-established pharmacological interventions including postnatal corticosteroids, early caffeine administration, and vitamin A. Recent advances in the clinical care of infants in the neonatal intensive care unit (NICU) have led to improvements in survival without a consistent reduction in the incidence of BPD. Our update provides latest insights from both preclinical models and clinical cohort studies and describes novel approaches to prevent BPD.Even more than 50 years after its initial description, bronchopulmonary dysplasia (BPD) remains one of the most important and lifelong sequelae following premature birth. Tremendous efforts have been undertaken since then to reduce this ever-increasing disease burden but a therapeutic breakthrough preventing BPD is still not in sight. The inflammatory response provoked in the immature lung is a key driver of distorted lung development and impacts the formation of alveolar, mesenchymal, and vascular structures during a particularly vulnerable time-period. During the last 5 years, new scientific insights have led to an improved pathomechanistic understanding of BPD origins and disease drivers. Within the framework of current scientific progress, concepts involving disruption of the balance of key inflammatory and lung growth promoting pathways by various stimuli, take center stage. Still today, the number of efficient therapeutics available to prevent BPD is limited to a few, well-established pharmacological interventions including postnatal corticosteroids, early caffeine administration, and vitamin A. Recent advances in the clinical care of infants in the neonatal intensive care unit (NICU) have led to improvements in survival without a consistent reduction in the incidence of BPD. Our update provides latest insights from both preclinical models and clinical cohort studies and describes novel approaches to prevent BPD. |
ArticleNumber | 7 |
Author | Schmidt, Annesuse Rivetti, Stefano Rekers, Lisa Selting, Ariane Dong, Ying Lauer, Tina Staude, Birte Zimmer, Klaus-Peter Holzfurtner, Lena Behnke, Judith Bellusci, Saverio Ehrhardt, Harald Shahzad, Tayyab |
Author_xml | – sequence: 1 givenname: Lena surname: Holzfurtner fullname: Holzfurtner, Lena organization: Department of General Pediatrics and Neonatology, Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Justus-Liebig-University – sequence: 2 givenname: Tayyab surname: Shahzad fullname: Shahzad, Tayyab organization: Department of General Pediatrics and Neonatology, Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Justus-Liebig-University – sequence: 3 givenname: Ying surname: Dong fullname: Dong, Ying organization: Department of General Pediatrics and Neonatology, Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Justus-Liebig-University – sequence: 4 givenname: Lisa surname: Rekers fullname: Rekers, Lisa organization: Department of General Pediatrics and Neonatology, Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Justus-Liebig-University – sequence: 5 givenname: Ariane surname: Selting fullname: Selting, Ariane organization: Department of General Pediatrics and Neonatology, Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Justus-Liebig-University – sequence: 6 givenname: Birte surname: Staude fullname: Staude, Birte organization: Department of General Pediatrics and Neonatology, Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Justus-Liebig-University – sequence: 7 givenname: Tina surname: Lauer fullname: Lauer, Tina organization: Department of General Pediatrics and Neonatology, Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Justus-Liebig-University – sequence: 8 givenname: Annesuse surname: Schmidt fullname: Schmidt, Annesuse organization: Department of General Pediatrics and Neonatology, Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Justus-Liebig-University – sequence: 9 givenname: Stefano surname: Rivetti fullname: Rivetti, Stefano organization: Department of Internal Medicine II, Universities of Giessen and Marburg Lung Center (UGMLC), Cardiopulmonary Institute (CPI), Member of the German Center for Lung Research (DZL), Justus-Liebig-University – sequence: 10 givenname: Klaus-Peter surname: Zimmer fullname: Zimmer, Klaus-Peter organization: Department of General Pediatrics and Neonatology, Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Justus-Liebig-University – sequence: 11 givenname: Judith surname: Behnke fullname: Behnke, Judith organization: Department of General Pediatrics and Neonatology, Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Justus-Liebig-University – sequence: 12 givenname: Saverio surname: Bellusci fullname: Bellusci, Saverio organization: Department of Internal Medicine II, Universities of Giessen and Marburg Lung Center (UGMLC), Cardiopulmonary Institute (CPI), Member of the German Center for Lung Research (DZL), Justus-Liebig-University – sequence: 13 givenname: Harald orcidid: 0000-0003-4587-1734 surname: Ehrhardt fullname: Ehrhardt, Harald email: Harald.Ehrhardt@paediat.med.uni-giessen.de organization: Department of General Pediatrics and Neonatology, Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Lung Research Center (DZL), Justus-Liebig-University |
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Keywords | Reactive oxygen species Bronchopulmonary dysplasia Inflammation Therapeutic approach Rodent Chronic lung disease Preterm Lung injury |
Language | English |
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PublicationTitle | Molecular and cellular pediatrics |
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Snippet | Even more than 50 years after its initial description, bronchopulmonary dysplasia (BPD) remains one of the most important and lifelong sequelae following... Abstract Even more than 50 years after its initial description, bronchopulmonary dysplasia (BPD) remains one of the most important and lifelong sequelae... |
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SubjectTerms | Alveoli Bronchopulmonary dysplasia Caffeine Chronic lung disease Complications Corticosteroids Diabetes Dysplasia Endocrinology Inflammation Lung diseases Lung injury Medicine Medicine & Public Health Mesenchyme Neonates Oncology Pediatrics Perinatal Origins of Chronic Lung Disease: Mechanisms - Prevention - Therapy Premature birth Preterm Reactive oxygen species Review Vitamin A |
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Title | When inflammation meets lung development—an update on the pathogenesis of bronchopulmonary dysplasia |
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