Regenerative therapy in nephrology. Repair or construction?

被引:1
作者
Haller, H. [1 ]
机构
[1] Hannover Med Sch, Klin Nieren & Hochdruckkrankheiten, Carl Neuberg Str 1, D-30625 Hannover, Germany
来源
INTERNIST | 2007年 / 48卷 / 08期
关键词
Regnerative medicine; Stem cell therapy; Chronic renal disease; Tubules; Dialysis;
D O I
10.1007/s00108-007-1910-1
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Animal experiments and analyses of human renal tissues show that regeneration of degraded renal tubules is caused by adjacent surviving tubules. Differentiation, migration, proliferation and redifferentiation are regulated by local growth factors. Renal stem cells can also participate in this process. Mesenchymal stem cells play a pivotal role in renal regeneration and if these are still present in the adult kidney, they could be the source material for repair and regeneration following injury. The exact location and role of resident mesenchymal stem cells which have been demonstrated in the kidneys is still unclear. New surface markers and a better characterisation of the many cell populations possibly participating in the regeneration process are necessary in order to clarify their complex interaction. It is also unclear whether mesenchymal stem cells from bone marrow or other organs are also involved. In addition to structural regeneration, the stem cells also play a role in the functional recovery following acute renal failure. Artificial regeneration of human kidneys is difficult due to their functional and spatial complexity. By the additional use of cells in dialysis machines it may be possible to improve the quality of filtration and also replace other renal functions. Initial results using this new technique in clinical phase I/II studies on patients with acute renal failure are promising.
引用
收藏
页码:813 / 818
页数:6
相关论文
共 46 条
[1]   Human mesenchymal stem cells modulate allogeneic immune cell responses [J].
Aggarwal, S ;
Pittenger, MF .
BLOOD, 2005, 105 (04) :1815-1822
[2]   In vivo contribution of murine mesenchymal stem cells into multiple cell-types under minimal damage conditions [J].
Anjos-Afonso, F ;
Siapati, EK ;
Bonnet, D .
JOURNAL OF CELL SCIENCE, 2004, 117 (23) :5655-5664
[3]   Dedifferentiation and proliferation of surviving epithelial cells in acute renal failure [J].
Bonventre, JV .
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2003, 14 (06) :S55-S61
[4]   Ischemic acute renal failure: An inflammatory disease? [J].
Bonventre, JV ;
Zuk, A .
KIDNEY INTERNATIONAL, 2004, 66 (02) :480-485
[5]   Isolation of renal progenitor cells from adult human kidney [J].
Bussolati, B ;
Bruno, S ;
Grange, C ;
Buttiglieri, S ;
Deregibus, MC ;
Cantino, D ;
Camussi, G .
AMERICAN JOURNAL OF PATHOLOGY, 2005, 166 (02) :545-555
[6]   Identifying the molecular phenotype of renal progenitor cells [J].
Challen, GA ;
Martinez, G ;
Davis, MJ ;
Taylor, DF ;
Crowe, M ;
Teasdale, RD ;
Grimmond, SM ;
Little, MH .
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2004, 15 (09) :2344-2357
[7]  
Dekel B, 2002, J AM SOC NEPHROL, V13, DOI 10.1681/ASN.V134977
[8]   Restoration of tubular epithelial cells during repair of the postischemic kidney occurs independently of bone marrow-derived stem cells [J].
Duffield, JS ;
Park, KM ;
Hsiao, LL ;
Kelley, VR ;
Scadden, DT ;
Ichimura, T ;
Bonventre, JV .
JOURNAL OF CLINICAL INVESTIGATION, 2005, 115 (07) :1743-1755
[9]   Nephrogenesis is induced by partial nephrectomy in the elasmobranch Leucoraja erinacea [J].
Elger, M ;
Hentschel, H ;
Litteral, J ;
Wellner, M ;
Kirsch, T ;
Luft, FC ;
Haller, H .
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2003, 14 (06) :1506-1518
[10]   Proliferation of bone marrow-derived cells contributes to regeneration after folic acid-induced acute tubular injury [J].
Fang, TC ;
Alison, MR ;
Cook, HT ;
Jeffery, R ;
Wright, NA ;
Poulsom, R .
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2005, 16 (06) :1723-1732