A Novel Insight Into the Mechanism of Pulmonary Hypertension Involving Caveolin-1 Deficiency and Endothelial Nitric Oxide Synthase Activation

You Yang Zhao*, Asrar B. Malik

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

33 Scopus citations

Abstract

Severe pulmonary hypertension (PH) is characterized by a progressive increase in pulmonary vascular resistance and vascular remodeling leading to right heart failure and early death. Our recent studies with the use of the novel mouse model with genetic deletions of caveolin-1 (Cav1) and endothelial nitric oxide synthase (eNOS) (NOS3) have demonstrated that persistent eNOS activation in Cav1-/- lungs results in tyrosine nitration of protein kinase G (PKG) and impairment of its activity, which thereby induces PH. The finding of eNOS activation and PKG nitration concomitant with Cav1 deficiency was recapitulated in lungs from patients with idiopathic pulmonary arterial hypertension. These data suggest targeting PKG nitration has potential value for the treatment of PH. Here, we will review the current knowledge about Cav1-regulated eNOS activity and its fundamental role in the pathogenesis of PH.

Original languageEnglish (US)
Pages (from-to)238-242
Number of pages5
JournalTrends in Cardiovascular Medicine
Volume19
Issue number7
DOIs
StatePublished - Oct 1 2009

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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