作者: Ralph Buttyan , Glenda Gobé
DOI: 10.1016/S1054-3589(08)61065-0
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摘要: In the preceding sections we have emphasized current status of our knowledge concerning involvement apoptosis in normal and abnormal renal developmental processes, control adult kidney size capacity, development disease states oncogenesis. At several points, noted that studies cells lag behind those other organ systems. Even with rudimentary now available, however, it is apparent an extremely important process kidney. Recent observations lend credence to view continued study this unique cell death might enable generation novel more effective therapies treat diseases malignancies. We wish highlight areas require particular attention. First, relationship between blood supply requires further investigation. Benign human are common population; know most these associated rates apoptosis. Although initiating agents for various vary, there good reason believe much occurs end result reduced flow initiated by causative agent. Cytokines or extrinsic can reduce apoptotic loss under conditions hold theoretical promise treating diseases. Second, urgent need define endocrine, paracrine, autocrine roles cytokines physiology pathogenesis syndromes. As indicated above, elaboration fibrous extracellular material fibroblasts tubulointerstitial regions appears be part final pathway leading end-stage disease. It understand how function controlled. Conversely, glomerular tubular also play a role many There already experimental clinical evidence showing IGF-1 hepatocyte growth factor useful [57, 58]. remains determined usefulness related their ability suppress as opposed promote true growth. Finally, analysis regulation during oncogenesis critical. Maligant cancers difficult detect adults before metastases cause symptoms; late stage tumors almost invariably fatal. The regress spontaneously indicates pathways retained cells, yet disappointing response chemotherapy learn about trigger pathways. Hopefully better understanding will lead improved therapy devastating group neoplasms.