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<p>Calcium oxalate (CaOx) nephrolithiasis is a globally prevalent disease with complex pathogenesis and limited targeted therapies. The imbalance between renal tubular epithelial cell (RTEC) injury and repair serves as a key driver of stone formation. Under hyperoxaluric or crystal-induced stress, RTECs undergo multiple regulated cell death pathways including apoptosis, pyroptosis, ferroptosis, and necroptosis, alongside autophagic dysfunction. These processes trigger the release of damage-associated molecular patterns and inflammatory mediators that amplify local inflammation and enhance crystal adhesion. Importantly, tubular repair after injury is not a uniform process but diverges into three distinct outcomes, including adaptive tubular regeneration, repair failure, and fibrogenic maladaptive repair. Persistent RTEC injury-repair imbalance disrupts tubular barrier integrity, perpetuates self-sustaining inflammatory cascades, and upregulates epithelial crystal adhesion molecules, collectively remodeling the renal microenvironment into a stable pro-stone niche that facilitates CaOx crystal deposition and stone formation. This review systematically summarizes the types of RTEC injury, the compromised repair pathways and their regulatory networks. It also discusses emerging therapeutic strategies aimed at correcting the injury-repair imbalance axis to provide new directions for the prevention and treatment of CaOx nephrolithiasis.</p>

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Renal tubular injury-repair imbalance in calcium oxalate nephrolithiasis: mechanisms and therapeutic implications

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月29日

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  • Shushuai Yang,
  • Yuanjiong Qi,
  • Shichao Zhang,
  • Longchao Zhang,
  • Qiuyu Yu,
  • Chenglong Xu,
  • Yue Chen,
  • Shiyong Qi

摘要

Calcium oxalate (CaOx) nephrolithiasis is a globally prevalent disease with complex pathogenesis and limited targeted therapies. The imbalance between renal tubular epithelial cell (RTEC) injury and repair serves as a key driver of stone formation. Under hyperoxaluric or crystal-induced stress, RTECs undergo multiple regulated cell death pathways including apoptosis, pyroptosis, ferroptosis, and necroptosis, alongside autophagic dysfunction. These processes trigger the release of damage-associated molecular patterns and inflammatory mediators that amplify local inflammation and enhance crystal adhesion. Importantly, tubular repair after injury is not a uniform process but diverges into three distinct outcomes, including adaptive tubular regeneration, repair failure, and fibrogenic maladaptive repair. Persistent RTEC injury-repair imbalance disrupts tubular barrier integrity, perpetuates self-sustaining inflammatory cascades, and upregulates epithelial crystal adhesion molecules, collectively remodeling the renal microenvironment into a stable pro-stone niche that facilitates CaOx crystal deposition and stone formation. This review systematically summarizes the types of RTEC injury, the compromised repair pathways and their regulatory networks. It also discusses emerging therapeutic strategies aimed at correcting the injury-repair imbalance axis to provide new directions for the prevention and treatment of CaOx nephrolithiasis.