Possible mechanisms of kidney repair.

Possible mechanisms of kidney repair.
复制标题

DOI:
10.1186/1755-1536-2-3
复制
发表时间:
2009-06-26
期刊:
Fibrogenesis & tissue repair
影响因子:
--
通讯作者:
Kalluri R
Kalluri R
中科院分区:
其他
文献类型:
--
作者:
Romagnani P;Kalluri R

文献摘要

被引文献

相似文献

在大多数成年上皮细胞中,通过干细胞/祖细胞的存在来维持替换受损或死亡细胞的过程,这使得上皮组织在损伤后得以修复。现有证据强烈支持成人肾脏中存在干细胞。事实上,最近的研究结果提供的证据,有利于内在的肾细胞的作用,反对骨髓来源的干细胞在肾上皮细胞再生的生理作用。此外,最近的研究已经在成人肾脏的Bowman囊内鉴定了CD 24 + CD 133+肾祖细胞的亚群,其为受损的肾上皮细胞提供再生潜力。有趣的是,CD 24 + CD 133+肾祖细胞也代表肾发育过程中肾小管细胞和足细胞的共同祖细胞。慢性损伤导致肾小管上皮细胞功能障碍,这触发了致纤维化细胞因子的释放和炎症细胞向受损肾脏的募集。瘢痕组织的快速插入可能通过防止感染性微生物侵入伤口而赋予生存优势,但阻止了随后的组织再生。然而,肾脏中肾上皮祖细胞的存在表明了对在实验动物甚至在人类中观察到的肾脏病变消退的可能解释。因此,为了使伤口修复过程向再生方向转变,对伤口修复过程的操纵可能需要减缓快速纤维化反应的能力,使得肾祖细胞可以允许组织再生而不是瘢痕形成。
In most adult epithelia the process of replacing damaged or dead cells is maintained through the presence of stem/progenitor cells, which allow epithelial tissues to be repaired following injury. Existing evidence strongly supports the presence of stem cells in the adult kidney. Indeed, recent findings provide evidence in favour of a role for intrinsic renal cells and against a physiological role for bone marrow-derived stem cells in the regeneration of renal epithelial cells. In addition, recent studies have identified a subset of CD24+CD133+ renal progenitors within the Bowman's capsule of adult human kidney, which provides regenerative potential for injured renal epithelial cells. Intriguingly, CD24+CD133+ renal progenitors also represent common progenitors of tubular cells and podocytes during renal development. Chronic injury causes dysfunction of the tubular epithelial cells, which triggers the release of fibrogenic cytokines and recruitment of inflammatory cells to injured kidneys. The rapid interposition of scar tissue probably confers a survival advantage by preventing infectious microorganisms from invading the wound, but prevents subsequent tissue regeneration. However, the existence of renal epithelial progenitors in the kidney suggests a possible explanation for the regression of renal lesions which has been observed in experimental animals and even in humans. Thus, manipulation of the wound repair process in order to shift it towards regeneration will probably require the ability to slow the rapid fibrotic response so that renal progenitor cells can allow tissue regeneration rather than scar formation.