Molecular mechanisms underlying hyperoxia-induced lung fibrosis

I. Ting Chen, Liang Ti Huang, Chih Cheng Chen, Chung Ming Chen

Research output: Contribution to journalReview articlepeer-review

Abstract

Supplemental oxygen is often used to treat newborns with respiratory disorders. Exposure to high concentration of oxygen and long-term oxygen causes inflammation and acute lung injury. The acute inflammatory phase is followed by a fibroproliferative repair phase, leading to lung fibrosis. Many infants with lung fibrosis develop significant respiratory morbidities including reactive airways dysfunction and obstructive lung disease during childhood. Despite the absence of effective treatments and the incomplete understanding regarding mechanisms underlying fibrosis, extensive literature regarding lung fibrosis from in vitro and in vivo hyperoxia-exposed models is available. In this review, we discuss molecular mediators and signaling pathways responsible for increased fibroblast proliferation and collagen production, excessive extracellular matrix accumulation, and eventually, lung fibrosis. We discuss each of these mediators separately to facilitate clear understanding as well as significant interactions occurring among these molecular mediators and signaling pathways.

Original languageEnglish
Pages (from-to)109-116
Number of pages8
JournalPediatrics and Neonatology
Volume63
Issue number2
DOIs
Publication statusPublished - Mar 2022

Keywords

  • collagen
  • cytokine
  • growth factor
  • reactive oxygen species
  • renin–angiotensin system

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health

Fingerprint

Dive into the research topics of 'Molecular mechanisms underlying hyperoxia-induced lung fibrosis'. Together they form a unique fingerprint.

Cite this