Role of Reactive Oxygen Species in Vascular Remodeling Associated with Pulmonary Hypertension

Stephen Wedgwood, Stephen M. Black

Research output: Contribution to journalReview article

64 Scopus citations

Abstract

Several manifestations of neonatal pulmonary hypertension are associated with vascular remodeling, resulting in increased muscularity of the small pulmonary arteries. Abnormal structural development of the pulmonary vasculature has been implicated in persistent pulmonary hypertension of the newborn (PPHN). Increased plasma levels of the vasoconstrictor endothelin-1 (ET-1) have been demonstrated in patients with PPHN, which is likely to contribute to hypertension. In addition, several studies have identified a role for ET-1 in the proliferation of vascular smooth muscle cells (SMCs), suggesting that ET-1 may also be involved in the vascular remodeling characteristic of this disease. However, the mechanisms of ET-1-induced SMC proliferation are unclear and appear to differ between cells from different origins within the vasculature. In SMCs isolated from fetal pulmonary arterial cells, ET-1 stimulated proliferation via an induction of reactive species (ROS). Furthermore, other lines of evidence have demonstrated the involvement of ROS in ET-1-stimulated SMC growth, suggesting that ROS may be a common factor in the mechanisms involved. This review discusses the potential roles for ROS in the abnormal pulmonary vascular development characteristic of PPHN, and the treatment strategies arising from our increasing knowledge of the molecular mechanisms involved.

Original languageEnglish (US)
Pages (from-to)759-769
Number of pages11
JournalAntioxidants and Redox Signaling
Volume5
Issue number6
DOIs
StatePublished - Dec 2003

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

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