Early injury of the neonatal lung contributes to premature lung aging: a hypothesis.

Silke Meiners,Anne Hilgendorff

doi:10.1186/s40348-016-0052-8

Abstract

Chronic lung disease of the newborn, also known as bronchopulmonary dysplasia (BPD), is the most common chronic lung disease in early infancy and results in an increased risk for long-lasting pulmonary impairment in the adult. BPD develops upon injury of the immature lung by oxygen toxicity, mechanical ventilation, and infections which trigger sustained inflammatory immune responses and extensive remodeling of the extracellular matrix together with dysregulated growth factor signaling. Histopathologically, BPD is characterized by impaired alveolarization, disrupted vascular development, and saccular wall fibrosis. Here, we explore the hypothesis that development of BPD involves disturbance of conserved pathways of molecular aging that may contribute to premature aging of the lung and an increased susceptibility to chronic lung diseases in adulthood.

Highlights

Chronic lung disease of the newborn, known as bronchopulmonary dysplasia (BPD), is the most common chronic lung disease in early infancy and results in an increased risk for pulmonary and neurologic impairment persisting into adulthood [1]
We propose that early alterations in major aging pathways drive premature aging of the lung thereby adding to the risk for development of chronic lung diseases later in life [9, 10]
Dysregulation of chromatin remodeling pathways including DNA methylation, histone acetylation, and miRNA regulation have been reported in response to hyperoxia in the neonatal lung in several experimental models and in BPD patients: The process of alveolar septation in the mouse and human lung is accompanied by altered DNA methylation profiles that coincide with distinct changes in gene expression

Summary

Introduction

Chronic lung disease of the newborn, known as bronchopulmonary dysplasia (BPD), is the most common chronic lung disease in early infancy and results in an increased risk for pulmonary and neurologic impairment persisting into adulthood [1]. We propose that early alterations in major aging pathways drive premature aging of the lung thereby adding to the risk for development of chronic lung diseases later in life [9, 10].

Results

Conclusion