Molecular mechanisms of pulmonary arterial remodeling

Patrick Crosswhite, Zhongjie Sun

Research output: Contribution to journalArticle

45 Citations (Scopus)

Abstract

Pulmonary arterial hypertension (PAH) is characterized by a persistent elevation of pulmonary arterial pressure and pulmonary arterial remodeling with unknown etiology. Current therapeutics available for PAH are primarily directed at reducing the pulmonary blood pressure through their effects on the endothelium. It is well accepted that pulmonary arterial remodeling is primarily due to excessive pulmonary arterial smooth muscle cell (PASMC) proliferation that leads to narrowing or occlusion of the pulmonary vessels. Future effective therapeutics will be successful in reversing the vascular remodeling in the pulmonary arteries and arterioles. The purpose of this review is to provide updated information on molecular mechanisms involved in pulmonary arterial remodeling with a focus on growth factors, transcription factors, and epigenetic pathways in PASMC proliferation. In addition, this review will highlight novel therapeutic strategies for potentially reversing PASMC proliferation.

Original languageEnglish (US)
Pages (from-to)191-201
Number of pages11
JournalMolecular Medicine
Volume20
Issue number1
DOIs
StatePublished - Jan 1 2014

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Lung
Smooth Muscle Myocytes
Cell Proliferation
Pulmonary Hypertension
Arterioles
Epigenomics
Pulmonary Artery
Endothelium
Vascular Remodeling
Intercellular Signaling Peptides and Proteins
Arterial Pressure
Transcription Factors
Therapeutics
Blood Pressure

All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Molecular Biology
  • Genetics
  • Genetics(clinical)

Cite this

Molecular mechanisms of pulmonary arterial remodeling. / Crosswhite, Patrick; Sun, Zhongjie.

In: Molecular Medicine, Vol. 20, No. 1, 01.01.2014, p. 191-201.

Research output: Contribution to journalArticle

Crosswhite, Patrick ; Sun, Zhongjie. / Molecular mechanisms of pulmonary arterial remodeling. In: Molecular Medicine. 2014 ; Vol. 20, No. 1. pp. 191-201.
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