【摘 要】
：
铁离子是胚胎肾发育的必需生长因子。妊娠妇女铁离子缺乏可导致胚胎肾发育缺陷,出生及成年后通常逐渐表现为慢性肾病。近来,我们建立了模拟妇女妊娠前后铁离子缺乏的小鼠模型和细胞特异性Tfr1基因敲除小鼠模型。研究结果发现,小鼠孕期前后铁离子缺乏可导致胚胎小肾甚至无肾,具体表现为胚胎肾的输尿管芽容量、肾小球和近端小管数目减少近90％；特异性敲除胚胎肾间充质、肾单位前体或输尿管芽细胞的铁离子转运基因Tfr1,
【机 构】
：
同济-长征医院转化医学研究中心、同济大学转化医学高等研究院和生命科学学院,上海,200092
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铁离子是胚胎肾发育的必需生长因子。妊娠妇女铁离子缺乏可导致胚胎肾发育缺陷,出生及成年后通常逐渐表现为慢性肾病。近来,我们建立了模拟妇女妊娠前后铁离子缺乏的小鼠模型和细胞特异性Tfr1基因敲除小鼠模型。研究结果发现,小鼠孕期前后铁离子缺乏可导致胚胎小肾甚至无肾,具体表现为胚胎肾的输尿管芽容量、肾小球和近端小管数目减少近90％；特异性敲除胚胎肾间充质、肾单位前体或输尿管芽细胞的铁离子转运基因Tfr1,可分别导致无肾、肾小球数目减少及出生后多囊肾或小肾。结论：这些研究说明铁离子缺乏直接影响胚胎肾细胞而导致缺陷且存在时空特异性,从而对于更科学合理、有效地早期预防和干预由铁离子缺乏导致的胚胎肾缺陷具有重要的理论指导意义。
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