The origin of interstitial myofibroblasts in chronic kidney disease.
The origin of interstitial myofibroblasts in chronic kidney disease.
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DOI：
10.1007/s00467-011-1772-6
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发表时间：
2012-02
影响因子：
3
通讯作者：
Humphreys, Benjamin D.
中科院分区：
文献类型：
--
作者：
Grgic, Ivica;Duffield, Jeremy S.;Humphreys, Benjamin D.
慢性肾脏疾病（CKD），独立于其主要原因，导致进行性的，不可逆的肾实质功能丧失。CKD的肾脏病理学特征为肾小管间质纤维化，伴有肌成纤维细胞产生的过度基质沉积。由于阻断这些瘢痕形成细胞的形成代表了进行性纤维化肾病患者的合理治疗目标，因此肾肌成纤维细胞的起源是一个深入研究的主题。虽然传统观点认为，居民成纤维细胞是肌成纤维细胞的前体，在过去的10年里，受伤的上皮细胞已被认为是直接有助于肌成纤维细胞池的上皮细胞间质转化（EMT）的过程。最近在小鼠纤维化模型中应用遗传命运作图技术为纤维化肾病的细胞层次结构提供了新的见解，结果对EMT是体内肌成纤维细胞募集来源的概念提出了质疑，而是指出常驻周细胞/血管周围成纤维细胞作为肌成纤维细胞祖细胞库。这篇综述将强调最近的研究结果，反对EMT作为一个直接贡献者的肾脏肌成纤维细胞的人口和审查使用的遗传命运映射来阐明肾脏稳态和疾病的细胞机制。
Chronic kidney diseases (CKD), independent of their primary cause, lead to progressive, irreversible loss of functional renal parenchyma. Renal pathology in CKD is characterized by tubulointerstitial fibrosis with excessive matrix deposition produced by myofibroblasts. Because blocking the formation of these scar-forming cells represents a logical therapeutic target for patients with progressive fibrotic kidney disease, the origin of renal myofibroblasts is a subject of intense investigation. Although the traditional view holds that resident fibroblasts are the myofibroblast precursor, for the last 10 years, injured epithelial cells have been thought to directly contribute to the myofibroblast pool by the process of epithelial-to-mesenchymal transition (EMT). The recent application of genetic fate mapping techniques in mouse fibrosis models has provided new insights into the cell hierarchies in fibrotic kidney disease and results cast doubt on the concept that EMT is a source of myofibroblast recruitment in vivo, but rather point to the resident pericyte/perivascular fibroblast as the myofibroblast progenitor pool. This review will highlight recent findings arguing against EMT as a direct contributor to the kidney myofibroblast population and review the use of genetic fate mapping to elucidate the cellular mechanisms of kidney homeostasis and disease.
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影响因子：
7.8
作者：
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通讯作者：
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影响因子：
6
作者：
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作者：
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DOI：
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发表时间：
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期刊：
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影响因子：
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作者：
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通讯作者：
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影响因子：
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作者：
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