Considering TWEAK as a target for therapy in renal and vascular injury

被引:56
作者
Ortiz, Alberto [1 ]
Belen Sanz, Ana [1 ]
Munoz Garcia, Begona [1 ]
Antonio Moreno, Juan [1 ]
Sanchez Nino, Maria Dolores [1 ]
Luis Martin-Ventura, Jose [1 ]
Egido, Jesus [1 ]
Miguel Blanco-Colio, Luis [1 ]
机构
[1] Univ Autonoma Madrid, Vasc & Renal Res Lab, Fdn Jimenez Diaz, Inst Reina Sofia Invest Nefrol, Madrid 28040, Spain
关键词
TWEAK; Fn14; receptor; Cytokines; TUMOR-NECROSIS-FACTOR; FACTOR-KAPPA-B; SMOOTH-MUSCLE-CELLS; FIBROBLAST GROWTH FACTOR-INDUCIBLE-14; ACUTE TUBULAR-NECROSIS; WEAK INDUCER; FAS LIGAND; MULTIFUNCTIONAL CYTOKINE; ATHEROSCLEROTIC PLAQUES; SCAVENGER RECEPTOR;
D O I
10.1016/j.cytogfr.2009.05.002
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
TWEAK is a cytokine of the TNF superfamily that activates the Fn14 receptor. TWEAK may regulate cell proliferation, cell death, cell differentiation, angiogenesis and inflammation. The expression of TWEAK and Fn14 is increased during vascular and renal injury. Inflammatory cytokines increase Fn14 receptor expression in tubular and vascular smooth muscle cells. Moreover, TWEAK induces tubular cell apoptosis under proinflammatory conditions. TWEAK itself contributes to renal and vascular inflammation by promoting chemokine and inflammatory cytokine secretion. Confirmation of its role in acute kidney injury and atherosclerotic lesions formation came from functional studies in experimental animal models. The available evidence suggests that TWEAK might be a target for therapeutic intervention in renal and vascular injury and its role in different forms of tissue damage should be further explored. (C) 2009 Elsevier Ltd. All rights reserved.
引用
收藏
页码:251 / 258
页数:8
相关论文
共 91 条
[1]   CD163-mediated hemoglobin-heme uptake activates macrophage HO-1, providing an antiinflammatory function [J].
Abraham, Nader G. ;
Drummond, George .
CIRCULATION RESEARCH, 2006, 99 (09) :911-914
[2]   IKKβ/2 induces TWEAK and apoptosis in mammary epithelial cells [J].
Baxter, Fiona O. ;
Came, Paul J. ;
Abell, Kathrine ;
Kedjouar, Blandine ;
Huth, Marion ;
Rajewsky, Klaus ;
Pasparakis, Manolis ;
Watson, Christine J. .
DEVELOPMENT, 2006, 133 (17) :3485-3494
[3]   Functions of NF-κB1 and NF-κB2 in immune cell biology [J].
Beinke, S ;
Ley, SC .
BIOCHEMICAL JOURNAL, 2004, 382 :393-409
[4]   TWEAK and Fn14.: New players in the pathogenesis of atherosclerosis [J].
Blanco-Colio, Luis M. ;
Martin-Ventura, Jose L. ;
Munoz-Garcia, Begona ;
Moreno, Juan A. ;
Meilhac, Olivier ;
Ortiz, Alberto ;
Egido, Jesus .
FRONTIERS IN BIOSCIENCE-LANDMARK, 2007, 12 :3648-3655
[5]   Identification of soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) as a possible biomarker of subclinical atherosclerosis [J].
Blanco-Colio, Luis M. ;
Martin-Ventura, Jose L. ;
Munoz-Garcia, Begona ;
Orbe, Josune ;
Paramo, Jose A. ;
Michel, Jean-Baptiste ;
Ortiz, Alberto ;
Meilhac, Olivier ;
Egido, Jesus .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2007, 27 (04) :916-922
[6]   The molecular architecture of the TNF superfamily [J].
Bodmer, JL ;
Schneider, P ;
Tschopp, J .
TRENDS IN BIOCHEMICAL SCIENCES, 2002, 27 (01) :19-26
[7]   Interactions of tumor necrosis factor (TNF) and TNF receptor family members in the mouse and human [J].
Bossen, Claudia ;
Ingold, Karine ;
Tardivel, Aubry ;
Bodmer, Jean-Luc ;
Gaide, Olivier ;
Hertig, Sylvie ;
Ambrose, Christine ;
Tschopp, Juerg ;
Schneider, Pascal .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2006, 281 (20) :13964-13971
[8]   The nuclear factor kappa-B signaling pathway participates in dysregulation of vascular smooth muscle cells in vitro and in human atherosclerosis [J].
Bourcier, T ;
Sukhova, G ;
Libby, P .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (25) :15817-15824
[9]   A previously unrecognized protein-protein interaction between TWEAK and CD163:: Potential biological implications [J].
Bover, Laura C. ;
Cardo-Vila, Marina ;
Kuniyasu, Akihiko ;
Sun, Jessica ;
Rangel, Roberto ;
Takeya, Motohiro ;
Aggarwal, Bharat B. ;
Arap, Wadih ;
Pasqualini, Renata .
JOURNAL OF IMMUNOLOGY, 2007, 178 (12) :8183-8194
[10]   Activated transcription factor nuclear factor-kappa B is present in the atherosclerotic lesion [J].
Brand, K ;
Page, S ;
Rogler, G ;
Bartsch, A ;
Brandl, R ;
Knuechel, R ;
Page, M ;
Kaltschmidt, C ;
Baeuerle, PA ;
Neumeier, D .
JOURNAL OF CLINICAL INVESTIGATION, 1996, 97 (07) :1715-1722