因应用不当或饮食污染摄入马兜铃酸I所引起的、以进展性间质纤维化为特征的急慢性肾炎称为马兜铃酸肾病或巴尔干地方性肾病。马兜铃酸I特异性损伤近端小管,而对肾脏其他组织细胞未表现出明显的直接损伤作用。因此,近曲小管上皮细胞通过有机阴离子蛋白1和3特异性摄入马兜铃酸I,是马兜铃酸I发挥特异性肾毒性作用的关键。近年来对肾小管摄取马兜铃酸I的机制已明确,但参与其在肾小管上皮细胞顶膜侧转运的蛋白鲜有报道。通过综述马兜铃酸I在肾小管的消除机制,以期为预防和治疗马兜铃酸肾病提供新靶点。

Acute and chronic nephritis characterised by progressive interstitial fibrosis caused by ingestion of aristolochic acid I through misapplication or dietary contamination is known as aristolochic acid nephropathy or Balkan endemic nephropathy.Aristolochic acid I specifically damages the proximal tubules, while it does not show any significant direct damaging effect on other tissue cells of the kidney. Therefore, the specific uptake of aristolochic acid I by proximal tubular epithelial cells via organic anionic proteins 1 and 3 is the key to the specific nephrotoxic effects of aristolochic acid I. The mechanism of renal tubular uptake of aristolochic acid I has been clarified in recent years, but the proteins involved in its transport on the apical side of renal tubular epithelial cells have rarely been reported. By reviewing the mechanism of aristolochic acid I elimination in renal tubules, we hope to provide new targets for the prevention and treatment of aristolochic acid nephropathy.

R969.1，R969.3

贵州省法医中药毒理学特色重点实验室项目(黔教合KY字[2021]004); 贵州省科技厅基础研究计划资助项目(黔科合基础-ZK[2022]一般465)