Lessons learned from cancer may help in the treatment of pulmonary hypertension.
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.
Adnot
Serge
S
INSERM U651 and Département de Physiologie, Hôpital H. Mondor, Assistance Publique des Hôpitaux de Paris, Créteil, France. serge.adnot@hmn.ap-hop-paris.fr
D000818:Animals; D017209:Apoptosis / Q000235:genetics; D005799:Genes, Dominant; D015316:Genetic Therapy / Q000379:methods; D006976:Hypertension, Pulmonary / Q000139:chemically induced / Q000235:genetics / Q000628:therapy*; D051034:Inhibitor of Apoptosis Proteins; D008869:Microtubule-Associated Proteins / Q000235:genetics* / Q000378:metabolism; D009154:Mutation; D009363:Neoplasm Proteins; D009369:Neoplasms / Q000235:genetics* / Q000378:metabolism; D011651:Pulmonary Artery / Q000378:metabolism; D051381:Rats; D000077022:Survivin
C107489:BIRC5 protein, human; D051034:Inhibitor of Apoptosis Proteins; D008869:Microtubule-Associated Proteins; D009363:Neoplasm Proteins; D000077022:Survivin