Targeting apoptosis in acute tubular injury

被引:60
作者
Ortiz, A
Justo, P
Sanz, A
Lorz, C
Egido, J
机构
[1] IRSIN, Nefrol Fundac Jimenez Diaz, Madrid 28040, Spain
[2] Univ Autonoma Madrid, Madrid 28040, Spain
关键词
apoptosis; kidney; acute renal failure; Bc12; death receptor; caspase;
D O I
10.1016/S0006-2952(03)00515-X
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Recent research has shown that apoptosis and its regulatory mechanisms contribute to cell number regulation in acute renal failure. Acute tubular necrosis is the most frequent form of parenchymal acute renal failure. The main causes are ischemia-reperfusion, sepsis and nephrotoxic drugs. Exogenous factors such as nephrotoxic drugs and bacterial products, and endogenous factors such as lethal cytokines promote tubular cell apoptosis. Such diverse stimuli engage intracellular death pathways that in some cases are stimulus-specific. We now review the role of apoptosis in acute renal failure, the potential molecular targets of therapeutic intervention, the therapeutic weapons to modulate the activity of these targets and the few examples of therapeutic intervention on apoptosis. (C) 2003 Elsevier Inc. All rights reserved.
引用
收藏
页码:1589 / 1594
页数:6
相关论文
共 37 条
[1]   Life-or-death decisions by the Bcl-2 protein family [J].
Adams, JM ;
Cory, S .
TRENDS IN BIOCHEMICAL SCIENCES, 2001, 26 (01) :61-66
[2]   Role of endogenous vascular endothelial growth factor in tubular cell protection against acute cyclosporine toxicity [J].
Arroyo, MVA ;
Suzuki, Y ;
Yagüe, S ;
Lorz, C ;
Jiménez, S ;
Soto, C ;
Barat, A ;
Belda, E ;
González-Pacheco, FR ;
Deudero, JJP ;
Castilla, MA ;
Egido, J ;
Ortiz, A ;
Caramelo, C .
TRANSPLANTATION, 2002, 74 (11) :1618-1624
[3]   Bcl-xL overexpression protects from apoptosis induced by HMG-CoA reductase inhibitors in murine tubular cells [J].
Blanco-Colio, LM ;
Justo, P ;
Daehn, I ;
Lorz, C ;
Ortiz, A ;
Egido, J .
KIDNEY INTERNATIONAL, 2003, 64 (01) :181-191
[4]  
Catalan MP, 2003, PERITON DIALYSIS INT, V23, P123
[5]  
Catalan MP, 2001, J AM SOC NEPHROL, V12, P2442, DOI 10.1681/ASN.V12112442
[6]   PROTECTION FROM FAS-MEDIATED APOPTOSIS BY A SOLUBLE FORM OF THE FAS MOLECULE [J].
CHENG, JH ;
ZHOU, T ;
LIU, CD ;
SHAPIRO, JP ;
BRAUER, MJ ;
KIEFER, MC ;
BARR, PJ ;
MOUNTZ, JD .
SCIENCE, 1994, 263 (5154) :1759-1762
[7]   Human renal organic anion transporter 1 (hOAT1) and its role in the nephrotoxicity of antiviral nucleotide analogs [J].
Cihlar, T ;
Ho, ES ;
Lin, DC ;
Mulato, AS .
NUCLEOSIDES NUCLEOTIDES & NUCLEIC ACIDS, 2001, 20 (4-7) :641-648
[8]   Inhibition of apoptosis induced by ischemia-reperfusion prevents inflammation [J].
Daemen, MARC ;
van't Veer, C ;
Denecker, G ;
Heemskerk, VH ;
Wolfs, TGAM ;
Clauss, M ;
Vandenabeele, P ;
Buurman, WA .
JOURNAL OF CLINICAL INVESTIGATION, 1999, 104 (05) :541-549
[9]   Organelle-specific initiation of cell death pathways [J].
Ferri, KF ;
Kroemer, G .
NATURE CELL BIOLOGY, 2001, 3 (11) :E255-E263
[10]   Apoptotic pathways: The roads to ruin [J].
Green, DR .
CELL, 1998, 94 (06) :695-698