CYTOKINES AND L-ARGININE IN RENAL INJURY AND REPAIR

被引:94
作者
KETTELER, M [1 ]
BORDER, WA [1 ]
NOBLE, NA [1 ]
机构
[1] UNIV UTAH, HLTH SCI CTR, DIV NEPHROL & HYPERTENS, SALT LAKE CITY, UT 84132 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY | 1994年 / 267卷 / 02期
关键词
TRANSFORMING GROWTH FACTOR-BETA; POLYAMINES; NITRIC OXIDE;
D O I
10.1152/ajprenal.1994.267.2.F197
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Advances in molecular biology have identified cytokines as mediators of pathophysiological changes in chronic renal disease. Transforming growth factor-beta (TGF-beta) plays an important role in the pathogenesis of glomerular and interstitial fibrosis, whereas platelet-derived growth factor (PDGF) is involved in proliferative changes in chronic progressive renal diseases. Tumor necrosis factor-alpha and interleukins are expressed in experimental models of renal disease and are causes of inflammation and cell migration. Cytokines act by many different mechanisms, and one target of their action may be L-arginine metabolism. Since the discovery of the effector molecule nitric oxide (NO), generated from L-arginine, knowledge of this pathway has increased dramatically. It became evident that the L-arginine/NO pathway is of major importance in the regulation of hemodynamics and neurotransmission, in host defense against intracellular microorganisms, and in immunologic tissue injury. This pathway is induced by proinflammatory cytokines and possibly regulated by TGF-P and PDGF. L-Arginine is also metabolized to L-ornithine, which can be processed to polyamines or to L-proline. As polyamines are important mediators of cell growth and L-proline is a substrate for collagen synthesis, both pathways, once activated, may be important in repair processes. It is likely that cytokines and L-arginine metabolism are interconnected and that both are involved in the inflammation, tissue repair, and fibrogenesis processes in the kidney. Dietary protein restriction in progressive renal diseases may substantially affect both systems. This review summarizes current knowledge about interactions of cytokines and L-arginine metabolism and the relevance to renal diseases.
引用
收藏
页码:F197 / F207
页数:11
相关论文
共 147 条
[91]   ROLE OF L-ARGININE-NITRIC OXIDE PATHWAY IN MYOCARDIAL REOXYGENATION INJURY [J].
MATHEIS, G ;
SHERMAN, MP ;
BUCKBERG, GD ;
HAYBRON, DM ;
YOUNG, HH ;
IGNARRO, LJ .
AMERICAN JOURNAL OF PHYSIOLOGY, 1992, 262 (02) :H616-H620
[92]   SUPPRESSION OF ARTHRITIS BY AN INHIBITOR OF NITRIC-OXIDE SYNTHASE [J].
MCCARTNEYFRANCIS, N ;
ALLEN, JB ;
MIZEL, DE ;
ALBINA, JE ;
XIE, QW ;
NATHAN, CF ;
WAHL, SM .
JOURNAL OF EXPERIMENTAL MEDICINE, 1993, 178 (02) :749-754
[93]  
MERIMEE TJ, 1965, LANCET, V2, P668
[94]  
MILLS CD, 1991, PROG CLIN BIOL RES, V365, P193
[95]  
MONCADA S, 1993, NEW ENGL J MED, V329, P2002
[96]  
MONCADA S, 1991, PHARMACOL REV, V43, P109
[97]   TISSUE-INJURY CAUSED BY DEPOSITION OF IMMUNE-COMPLEXES IS L-ARGININE DEPENDENT [J].
MULLIGAN, MS ;
HEVEL, JM ;
MARLETTA, MA ;
WARD, PA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (14) :6338-6342
[98]   EXPRESSION OF NITRIC-OXIDE SYNTHASE IN KIDNEY MACULA DENSA CELLS [J].
MUNDEL, P ;
BACHMANN, S ;
BADER, M ;
FISCHER, A ;
KUMMER, W ;
MAYER, B ;
KRIZ, W .
KIDNEY INTERNATIONAL, 1992, 42 (04) :1017-1019
[99]   MESSENGER-RNA EXPRESSION OF GROWTH-FACTORS IN GLOMERULI FROM DIABETIC RATS [J].
NAKAMURA, T ;
FUKUI, M ;
EBIHARA, I ;
OSADA, S ;
NAGAOKA, I ;
TOMINO, Y ;
KOIDE, H .
DIABETES, 1993, 42 (03) :450-456
[100]   MESSENGER-RNA EXPRESSION FOR GROWTH-FACTORS IN GLOMERULI FROM FOCAL GLOMERULAR SCLEROSIS [J].
NAKAMURA, T ;
EBIHARA, I ;
FUKUI, M ;
OSADA, S ;
NAGAOKA, I ;
HORIKOSHI, S ;
TOMINO, Y ;
KOIDE, H .
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY, 1993, 66 (01) :33-42