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 inMolecular and cellular pediatrics Vol. 9; no. 1; pp. 7 - 12
Main Authors Holzfurtner, Lena, Shahzad, Tayyab, Dong, Ying, Rekers, Lisa, Selting, Ariane, Staude, Birte, Lauer, Tina, Schmidt, Annesuse, Rivetti, Stefano, Zimmer, Klaus-Peter, Behnke, Judith, Bellusci, Saverio, Ehrhardt, Harald
Format Journal Article
LanguageEnglish
Published Cham Springer International Publishing 20.04.2022
Springer Nature B.V
SpringerOpen
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ISSN2194-7791
2194-7791
DOI10.1186/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.
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
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Issue 1
Keywords Reactive oxygen species
Bronchopulmonary dysplasia
Inflammation
Therapeutic approach
Rodent
Chronic lung disease
Preterm
Lung injury
Language English
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PublicationCentury 2000
PublicationDate 2022-04-20
PublicationDateYYYYMMDD 2022-04-20
PublicationDate_xml – month: 04
  year: 2022
  text: 2022-04-20
  day: 20
PublicationDecade 2020
PublicationPlace Cham
PublicationPlace_xml – name: Cham
– name: Germany
– name: Heidelberg
PublicationTitle Molecular and cellular pediatrics
PublicationTitleAbbrev Mol Cell Pediatr
PublicationTitleAlternate Mol Cell Pediatr
PublicationYear 2022
Publisher Springer International Publishing
Springer Nature B.V
SpringerOpen
Publisher_xml – name: Springer International Publishing
– name: Springer Nature B.V
– name: SpringerOpen
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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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