Lessons learned from cancer may help in the treatment of pulmonary hypertension

被引:37
作者
Adnot, S [1 ]
机构
[1] INSERM, Fac Med, Dept Physiol, U651, F-94010 Creteil, France
[2] Hop Henri Mondor, Assistance Publ Hop Paris, Dept Physiol, F-94010 Creteil, France
关键词
D O I
10.1172/JCI25399
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
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 (see the related article beginning on page 1479). 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.
引用
收藏
页码:1461 / 1463
页数:3
相关论文
共 18 条
[1]   Validating survivin as a cancer therapeutic target [J].
Altieri, DC .
NATURE REVIEWS CANCER, 2003, 3 (01) :46-54
[2]   Primary pulmonary hypertension is associated with reduced pulmonary vascular expression of type II bone morphogenetic protein receptor [J].
Atkinson, C ;
Stewart, S ;
Upton, PD ;
Machado, R ;
Thomson, JR ;
Trembath, RC ;
Morrell, NW .
CIRCULATION, 2002, 105 (14) :1672-1678
[3]   Inhibitor of apoptosis protein survivin regulates vascular injury [J].
Blanc-Brude, OP ;
Yu, J ;
Simosa, H ;
Conte, MS ;
Sessa, WC ;
Altieri, DC .
NATURE MEDICINE, 2002, 8 (09) :987-994
[4]   Survivin-dependent angiogenesis in ischemic brain - Molecular mechanisms of hypoxia-induced up-regulation [J].
Conway, EM ;
Zwerts, F ;
Van Eygen, V ;
DeVriese, A ;
Nagai, N ;
Luo, W ;
Collen, D .
AMERICAN JOURNAL OF PATHOLOGY, 2003, 163 (03) :935-946
[5]   Familial primary pulmonary hypertension (gene PPH1) is caused by mutations in the bone morphogenetic protein receptor-II gene [J].
Deng, ZM ;
Morse, JH ;
Slager, SL ;
Cuervo, N ;
Moore, KJ ;
Venetos, G ;
Kalachikov, S ;
Cayanis, E ;
Fischer, SG ;
Barst, RJ ;
Hodge, SE ;
Knowles, JA .
AMERICAN JOURNAL OF HUMAN GENETICS, 2000, 67 (03) :737-744
[6]   Pathobiology of pulmonary arterial hypertension [J].
Eddahibi, S ;
Morrell, N ;
D'Ortho, MP ;
Naeije, R ;
Adnot, S .
EUROPEAN RESPIRATORY JOURNAL, 2002, 20 (06) :1559-1572
[7]  
Eddahibi S, 2001, J CLIN INVEST, V108, P1141, DOI 10.1172/JCI200112805
[8]  
Kato J, 2001, INT J CANCER, V95, P92
[9]   Heterozygous germline mutations in BMPR2, encoding a TGF-β receptor, cause familial primary pulmonary hypertension [J].
Lane, KB ;
Machado, RD ;
Pauciulo, MW ;
Thomson, JR ;
Phillips, JA ;
Loyd, JE ;
Nichols, WC ;
Trembath, RC .
NATURE GENETICS, 2000, 26 (01) :81-84
[10]   Monoclonal endothelial cell proliferation is present in primary but not secondary pulmonary hypertension [J].
Lee, SD ;
Shroyer, KR ;
Markham, NE ;
Cool, CD ;
Voelkel, NF ;
Tuder, RM .
JOURNAL OF CLINICAL INVESTIGATION, 1998, 101 (05) :927-934