Renal studies provide an insight into cardiac extracellular matrix remodeling during health and disease

被引:10
作者
Hertig, Alexandre
Gangadhar, Taduri
Kalluri, Raghu [1 ,2 ]
机构
[1] Harvard Univ, Beth Israel Deaconess Med Ctr, Dept Med, Sch Med,Div Matrix Biol,Ctr Life Sci, Boston, MA 02115 USA
[2] Harvard Mit Div Hlth Sci & Technol, Boston, MA USA
关键词
Extra-cellular matrix; Heart remodeling; Acute kidney injury; Fibrosis; Epithelial to mesenchymal transition; Endothelial to mesenchymal transition; Integrin; tPA; PAI-1; Transforming growth factor beta; TO-MESENCHYMAL TRANSITION; MYOCARDIAL-INFARCTION; INTERSTITIAL FIBROSIS; KIDNEY-TRANSPLANTS; FIBROBLASTS DERIVE; PROGENITOR CELLS; RISK-FACTORS; INTEGRIN; GENE; FAILURE;
D O I
10.1016/j.yjmcc.2009.07.022
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The remodeling of a heart ventricle after myocardial infarction involves numerous inflammatory mediators that may trigger a long-lasting and a highly fibrogenic process. Likewise, in the kidney, acute and chronic injuries may lead to abnormal extracellular matrix deposition and eventually lead to the loss of renal function. Major breakthroughs have emerged during the last ten years with respect to the pathophysiology of matrix remodeling. Epithelial and endothelial cells are plastic, and able to engage in epithelial (or endothelial)-to-mesenchymal transition (EMT or EndMT), thus actively contributing to the fibrogenesis. Members of the fibrinolytic system were demonstrated to possess unsuspected properties and interact with receptors and integrins on endothelial and epithelial cells. Finally, a notion that stem cells could integrate into damaged tissue has recently emerged, which likely contributes to the tissue repair. In many aspects, the kidney and the heart share many common injury mechanisms. We envision that some of them will be accessible as common therapeutic targets in the future. (C) 2009 Elsevier Ltd. All rights reserved.
引用
收藏
页码:497 / 503
页数:7
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共 50 条
[1]   Epithelial-mesenchymal transitions: the importance of changing cell state in development and disease [J].
Acloque, Herve ;
Adams, Meghan S. ;
Fishwick, Katherine ;
Bronner-Fraser, Marianne ;
Angela Nieto, M. .
JOURNAL OF CLINICAL INVESTIGATION, 2009, 119 (06) :1438-1449
[2]  
Anavekar NS, 2004, NEW ENGL J MED, V351, P1285, DOI 10.1056/NEJMoa041365
[3]   Transcoronary transplantation of progenitor cells after myocardial infarction [J].
Assmus, Birgit ;
Honold, Joerg ;
Schaechinger, Volker ;
Britten, Martina B. ;
Fischer-Rasokat, Ulrich ;
Lehmann, Ralf ;
Teupe, Claudius ;
Pistorius, Katrin ;
Martin, Hans ;
Abolmaali, Nasreddin D. ;
Tonn, Torsten ;
Dimmeler, Stefanie ;
Zeiher, Andreas M. .
NEW ENGLAND JOURNAL OF MEDICINE, 2006, 355 (12) :1222-1232
[4]   Kidney-heart interactions: Epidemiology, pathogenesis, and treatment [J].
Berl, Tomas ;
Henrich, William .
CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2006, 1 (01) :8-18
[5]   Regression of renal vascular and glomerular fibrosis: Role of angiotensin II receptor antagonism and matrix metalloproteinases [J].
Boffa, JJ ;
Lu, Y ;
Placier, S ;
Stefanski, A ;
Dussaule, JC ;
Chatziantoniou, C .
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2003, 14 (05) :1132-1144
[6]   Plasmin is not protective in experimental renal interstitial fibrosis [J].
Edgtton, KL ;
Gow, RM ;
Kelly, DJ ;
Carmeliet, P ;
Kitching, AR .
KIDNEY INTERNATIONAL, 2004, 66 (01) :68-76
[7]   Reversal of lesions of diabetic nephropathy after pancreas transplantation [J].
Fioretto, P ;
Steffes, MW ;
Sutherland, DER ;
Goetz, FC ;
Mauer, M .
NEW ENGLAND JOURNAL OF MEDICINE, 1998, 339 (02) :69-75
[8]   The plasminogen-MMP system is more activated in the scar than in viable myocardium 3 months post-MI in the rat [J].
Gaertner, R ;
Jacob, MP ;
Prunier, F ;
Angles-Cano, E ;
Mercadier, JJ ;
Michel, JB .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2005, 38 (01) :193-204
[9]   Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization [J].
Go, AS ;
Chertow, GM ;
Fan, DJ ;
McCulloch, CE ;
Hsu, CY .
NEW ENGLAND JOURNAL OF MEDICINE, 2004, 351 (13) :1296-1305
[10]   αvβ6 integrin regulates renal fibrosis and inflammation in Alport mouse [J].
Hahm, Kyungmin ;
Lukashev, Matvey E. ;
Luo, Yi ;
Yang, William J. ;
Dolinski, Brian M. ;
Weinreb, Paul H. ;
Simon, Kenneth J. ;
Wang, Li Chun ;
Leone, Diane R. ;
Lobb, Roy R. ;
McCrann, Donald J. ;
Allaire, Normand E. ;
Horan, Gerald S. ;
Fogo, Agnes ;
Kalluri, Raghu ;
Shield, Charles F., III ;
Sheppard, Dean ;
Gardner, Humphrey A. ;
Violette, Shelia M. .
AMERICAN JOURNAL OF PATHOLOGY, 2007, 170 (01) :110-125