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<p>Ureteral stricture is a common complication in urological practice. However, many existing animal models cause excessive tissue damage or exhibit inconsistent healing; consequently, the pathogenesis of clinical ureteral stricture of mechanical origin is not accurately reproduced. This study aimed to establish a rat model of ureteral scar stricture induced by mechanical injury and to characterize its morphological and molecular features. Adult male Sprague–Dawley rats underwent left ureteral occlusion using a micro-hemostatic clamp for 12&#xa0;h. Renal morphology and function were evaluated by color Doppler ultrasound at 4, 6, and 8&#xa0;weeks after surgery. Pathological and molecular changes in the injured ureter and ipsilateral kidney were assessed by histopathology, immunohistochemistry, reverse transcription quantitative PCR (RT-qPCR), and Western blot (WB). Progressive hydronephrosis of the left renal pelvis was observed over time. Marked fibroblast proliferation and collagen deposition were noted in the injured ureteral segment. Expression levels of alpha-smooth muscle actin (α-SMA), collagen type I (Col Ⅰ) and collagen type III (Col Ⅲ), fibronectin (FN), and SMAD3/p-SMAD3 were significantly increased. These findings suggest that mechanical ureteral injury induces a typical fibrotic response and leads to scar stricture formation. This model appears to reliably mimic the development and progression of ureteral stricture and may provide a useful platform for further studies on the mechanisms of ureteral scar formation, as well as for the development of preventive and therapeutic strategies.</p>

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Establishment and characterization of a rat model of ureteral scar stricture induced by mechanical injury

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月19日

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  • Aobing Mei,
  • Qiangqiang Cheng,
  • Miaoqing Cai,
  • Chaokai Pu,
  • Lei Liu,
  • Tingtao Hu,
  • Xijun Wu,
  • Xu Sun

摘要

Ureteral stricture is a common complication in urological practice. However, many existing animal models cause excessive tissue damage or exhibit inconsistent healing; consequently, the pathogenesis of clinical ureteral stricture of mechanical origin is not accurately reproduced. This study aimed to establish a rat model of ureteral scar stricture induced by mechanical injury and to characterize its morphological and molecular features. Adult male Sprague–Dawley rats underwent left ureteral occlusion using a micro-hemostatic clamp for 12 h. Renal morphology and function were evaluated by color Doppler ultrasound at 4, 6, and 8 weeks after surgery. Pathological and molecular changes in the injured ureter and ipsilateral kidney were assessed by histopathology, immunohistochemistry, reverse transcription quantitative PCR (RT-qPCR), and Western blot (WB). Progressive hydronephrosis of the left renal pelvis was observed over time. Marked fibroblast proliferation and collagen deposition were noted in the injured ureteral segment. Expression levels of alpha-smooth muscle actin (α-SMA), collagen type I (Col Ⅰ) and collagen type III (Col Ⅲ), fibronectin (FN), and SMAD3/p-SMAD3 were significantly increased. These findings suggest that mechanical ureteral injury induces a typical fibrotic response and leads to scar stricture formation. This model appears to reliably mimic the development and progression of ureteral stricture and may provide a useful platform for further studies on the mechanisms of ureteral scar formation, as well as for the development of preventive and therapeutic strategies.