Hyperplasia of pulmonary artery SMCs (PASMCs) is a pathological hallmark of pulmonary arterial hypertension (PAH). In this issue of the JCI, McMurtry et al. report that adenovirus-mediated overexpression of survivin — a multipotent inhibitor of apoptosis — induces PAH in rats, whereas inhalation of an adenovirus vector encoding a mutant survivin gene with dominant-negative properties reverses established monocrotaline-induced PAH. These findings raise important issues regarding the role of survivin in the pathogenesis of PAH, its value as a prognostic indicator, and its use as a target for new therapeutic strategies.
Serge Adnot
Title and authors | Publication | Year |
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Rapamycin Reverses Pulmonary Artery Smooth Muscle Cell Proliferation in Pulmonary Hypertension
A Houssaini, S Abid, N Mouraret, F Wan, D Rideau, M Saker, E Marcos, CM Tissot, JL Dubois-Randé, V Amsellem, S Adnot |
American journal of respiratory cell and molecular biology | 2013 |