The Pathophysiology of the Peritoneal Membrane

被引:224
作者
Devuyst, Olivier [1 ]
Margetts, Peter J. [2 ]
Topley, Nicholas [3 ]
机构
[1] UCL Med Sch, Div Nephrol, B-1200 Brussels, Belgium
[2] McMaster Univ, Dept Med, St Josephs Hosp, Hamilton, ON, Canada
[3] Cardiff Univ, Sch Med, Dept Infect Immun & Biochem, Cardiff, S Glam, Wales
来源
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY | 2010年 / 21卷 / 07期
基金
英国医学研究理事会; 英国惠康基金; 加拿大健康研究院;
关键词
NITRIC-OXIDE SYNTHASE; EPITHELIAL-MESENCHYMAL TRANSITION; GROWTH-FACTOR-BETA; MESOTHELIAL CELLS; STRUCTURAL MODIFICATIONS; PERMEABILITY CHANGES; WATER PERMEABILITY; ANIMAL-MODELS; RAT MODEL; DIALYSIS;
D O I
10.1681/ASN.2009070694
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
The development of peritoneal dialysis (PD) as a successful therapy has and still depends on experimental models to test and understand critical pieces of pathophysiology. To date, the majority of studies performed in rat and rabbit models derive mechanistic insights primarily on the basis of interventional pharmacologic agents, blocking antibodies, or transient expression systems. Because body size no longer limits the performance of in vivo studies of PD, genetic mouse models are increasingly available to investigate the molecular and pathophysiologic mechanisms of the peritoneal membrane. We illustrate in this review how these investigations are catching up with other areas of biomedical research and provide direct evidence for understanding transport and ultrafiltration, responses to infection, and structural changes including fibrosis and angiogenesis These studies are relevant to mechanisms responsible not only for the major complications of PD but also for endothelial biology, host defense, inflammation, and tissue repair processes.
引用
收藏
页码:1077 / 1085
页数:9
相关论文
共 79 条
[21]  
Devuyst O., 2009, NOLPH GOKALS TXB PER, P757
[22]   Are phospholipase A2 and nitric oxide involved in the alterations in peritoneal transport during CAPD peritonitis? [J].
Douma, CE ;
de Waart, DR ;
Struijk, DG ;
Krediet, RT .
JOURNAL OF LABORATORY AND CLINICAL MEDICINE, 1998, 132 (04) :329-340
[23]   New functions for the matrix metalloproteinases in cancer progression [J].
Egeblad, M ;
Werb, Z .
NATURE REVIEWS CANCER, 2002, 2 (03) :161-174
[24]   Inhibition of nitric oxide synthase reverses changes in peritoneal permeability in a rat model of acute peritonitis [J].
Ferrier, ML ;
Combet, S ;
van Landschoot, M ;
Stoenoiu, MS ;
Cnops, Y ;
Lameire, N ;
Devuyst, O .
KIDNEY INTERNATIONAL, 2001, 60 (06) :2343-2350
[25]  
FORSTERMANN U, 1995, N-S ARCH PHARMACOL, V352, P351
[26]  
Garosi G, 2009, CONTRIB NEPHROL, V163, P45, DOI 10.1159/000223779
[27]  
GOLTOIB L, 2009, NOLPH GOKALS TXB PER, P73
[28]   ESRD patients in 2004: global overview of patient numbers, treatment modalities and associated trends [J].
Grassmann, A ;
Gioberge, S ;
Moeller, S ;
Brown, G .
NEPHROLOGY DIALYSIS TRANSPLANTATION, 2005, 20 (12) :2587-2593
[29]  
Ha HJ, 2000, PERITON DIALYSIS INT, V20, pS15
[30]   Insulin-like growth factor binding protein-5 is a target of matrix metalloproteinase-7: Implications for epithelial-mesenchymal signaling [J].
Hemers, E ;
Duval, C ;
McCaig, C ;
Handley, M ;
Dockray, GJ ;
Varro, A .
CANCER RESEARCH, 2005, 65 (16) :7363-7369