Bard J B, Woolf A S
MRC Human Genetics Unit, Western General Hospital, Edinburgh, UK.
Nephrol Dial Transplant. 1992;7(7):563-72. doi: 10.1093/ndt/7.7.563.
Over the last few years there has been considerable progress in analysing the cellular basis of nephrogenesis and a start has been made towards elucidating the underlying molecular controls of this process. In this review we begin by describing how the kidney forms and then consider recent work on the mechanisms underlying these events. We review evidence implicating a neural basis for kidney induction and go on to show how the induced metanephric mesenchyme aggregates and forms condensations which themselves polarize to form epithelia and filtering nephrons. We then discuss how changes in the extracellular matrix are implicated in these processes and how the expression of nuclear transcription factors may regulate the final phenotype of the kidney. Finally, we show how the study of nephrogenesis is beginning to shed light on the aetiology of a range of disorders that include renal malformations, renal tumours, and inherited glomerular and polycystic kidney diseases.
在过去几年中，在分析肾发生的细胞基础方面取得了相当大的进展，并且已经开始着手阐明这一过程的潜在分子调控机制。在这篇综述中，我们首先描述肾脏是如何形成的，然后探讨这些事件背后机制的近期研究成果。我们回顾了暗示肾脏诱导存在神经基础的证据，并继续展示诱导的后肾间充质如何聚集并形成凝集体，这些凝集体自身极化形成上皮和滤过性肾单位。接着，我们讨论细胞外基质的变化如何参与这些过程，以及核转录因子的表达如何调控肾脏的最终表型。最后，我们展示了肾发生的研究如何开始揭示一系列疾病的病因，这些疾病包括肾畸形、肾肿瘤以及遗传性肾小球疾病和多囊肾病。
