Angiogenesis and hereditary hemorrhagic telangiectasia -: Rendu-Osler-Weber disease

被引:11
作者
Sabbà, C
Cirulli, A
Rizzi, R
Pasculli, G
Gallitelli, M
Specchia, G
Liso, V
机构
[1] Univ Bari, Cattedra Ematol, Unita Operat Ematol, I-70124 Bari, Italy
[2] Univ Bari, Cattedra Med Urgenza & Pronto Soccorso, I-70124 Bari, Italy
关键词
angiogenesis; Rendu-Osler-Weber disease; telangiectasia;
D O I
10.1159/000046618
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
To date much of the recent work on pathological angiogenesis has focused on inflammatory diseases, diabetes and cancer in particular. Hereditary hemorrhagic telangiectasia or Rendu-Osler-Weber disease provides an example of the genetic disorder of angiogenesis in which a multisystemic angiodysplasia is responsible for severe hemorrhage. The disease pathogenesis is partially explained by a defect in the TGF-beta signaling system, although in more recent works a possible role of other vascular growth factors has been proposed. This paper provides a model of an aberrant angiogenesis in which multiple vascular growth factors could be involved in a diffuse angiodysplasia. Copyright (C) 2001 S. Karger AG, Basel.
引用
收藏
页码:214 / 219
页数:6
相关论文
共 48 条
[1]   IDENTIFICATION OF HUMAN ACTIVIN AND TGF-BETA TYPE-I RECEPTORS THAT FORM HETEROMERIC KINASE COMPLEXES WITH TYPE-II RECEPTORS [J].
ATTISANO, L ;
CARCAMO, J ;
VENTURA, F ;
WEIS, FMB ;
MASSAGUE, J ;
WRANA, JL .
CELL, 1993, 75 (04) :671-680
[2]  
Azuma Hiroyuki, 2000, Journal of Medical Investigation, V47, P81
[3]   Endoglin is an accessory protein that interacts with the signaling receptor complex of multiple members of the transforming growth factor-β superfamily [J].
Barbara, NP ;
Wrana, JL ;
Letarte, M .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (02) :584-594
[4]   A TRANSFORMING GROWTH-FACTOR-BETA TYPE-I RECEPTOR THAT SIGNALS TO ACTIVATE GENE-EXPRESSION [J].
BASSING, CH ;
YINGLING, JM ;
HOWE, DJ ;
WANG, TW ;
HE, WW ;
GUSTAFSON, ML ;
SHAH, P ;
DONAHOE, PK ;
WANG, XF .
SCIENCE, 1994, 263 (5143) :87-89
[5]   IDENTIFICATION AND EXPRESSION OF 2 FORMS OF THE HUMAN TRANSFORMING GROWTH FACTOR-BETA-BINDING PROTEIN ENDOGLIN WITH DISTINCT CYTOPLASMIC REGIONS [J].
BELLON, T ;
CORBI, A ;
LASTRES, P ;
CALES, C ;
CEBRIAN, M ;
VERA, S ;
CHEIFETZ, S ;
MASSAGUE, J ;
LETARTE, M ;
BERNABEU, C .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1993, 23 (09) :2340-2345
[6]   Endoglin expression is reduced in normal vessels but still detectable in arteriovenous malformations of patients with hereditary hemorrhagic telangiectasia type 1 [J].
Bourdeau, A ;
Cymerman, U ;
Paquet, ME ;
Meschino, W ;
McKinnon, WC ;
Guttmacher, AE ;
Becker, L ;
Letarte, M .
AMERICAN JOURNAL OF PATHOLOGY, 2000, 156 (03) :911-923
[7]   A murine model of hereditary hemorrhagic telangiectasia [J].
Bourdeau, A ;
Dumont, DJ ;
Letarte, M .
JOURNAL OF CLINICAL INVESTIGATION, 1999, 104 (10) :1343-1351
[8]   ULTRASTRUCTURE AND 3-DIMENSIONAL ORGANIZATION OF THE TELANGIECTASES OF HEREDITARY HEMORRHAGIC TELANGIECTASIA [J].
BRAVERMAN, IM ;
KEH, A ;
JACOBSON, BS .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1990, 95 (04) :422-427
[9]   PHYSIOLOGICAL CONSEQUENCES OF LOSS OF PLASMINOGEN-ACTIVATOR GENE-FUNCTION IN MICE [J].
CARMELIET, P ;
SCHOONJANS, L ;
KIECKENS, L ;
REAM, B ;
DEGEN, J ;
BRONSON, R ;
DEVOS, R ;
VANDENOORD, JJ ;
COLLEN, D ;
MULLIGAN, RC .
NATURE, 1994, 368 (6470) :419-424
[10]   SPECIFIC BINDING OF ENDOCRINE TRANSFORMING GROWTH-FACTOR-BETA-1 TO VASCULAR ENDOTHELIUM [J].
DICKSON, K ;
PHILIP, A ;
WARSHAWSKY, H ;
OCONNORMCCOURT, M ;
BERGERON, JJM .
JOURNAL OF CLINICAL INVESTIGATION, 1995, 95 (06) :2539-2554