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<p>Anticancer therapy-related renal injury (ATRI) has become increasingly prominent as contemporary oncology extends survival and intensifies combination regimens. Conventional chemotherapeutics, molecular targeted agents, immune checkpoint inhibitors, and immune cell-based therapies can induce distinct patterns of kidney injury, including proximal tubular toxicity with acute kidney injury, glomerular endothelial injury with proteinuria or thrombotic microangiopathy, immune-mediated acute interstitial nephritis, and systemic inflammatory or hemodynamic injury associated with cellular immunotherapy. Current management relies mainly on monitoring, supportive care, dose modification, and immunosuppression when indicated, yet these approaches are often reactive and may compromise anticancer treatment intensity. Therefore, effective strategies that preserve nephron structure and function without weakening antitumor efficacy remain an unmet need. Importantly, despite compelling biological rationale, no cell-based or cell-derived therapy has yet demonstrated improved long-term renal outcomes or overall survival in randomized trials involving cancer patients with ATRI. Cell-based and cell-derived therapies represent a promising direction for onco-nephroprotection by integrating immunomodulation, trophic support, and regenerative repair. Mesenchymal stem cells mainly act through paracrine programs to restrain inflammation, enhance tubular cell survival, and limit fibrotic remodeling, although limited renal delivery and oncologic safety remain major barriers. Renal progenitor and precursor cell strategies aim to promote structural repair but require strict control of cell purity, differentiation stage, and genomic stability. Exosomes are emerging as cell-free modalities, yet their cargo heterogeneity and context-dependent effects in tumor biology require careful evaluation. This mini review summarizes ATRI mechanisms, the rationale and evidence for major cellular platforms, and future directions for biomarker-guided translation.</p>

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Cell-based and cell-derived strategies for anticancer therapy-related renal injury: progress, challenges, and translational perspectives

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月31日

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  • Zixuan Chen,
  • Yiwei Xie,
  • Hua Sun,
  • Min Liu

摘要

Anticancer therapy-related renal injury (ATRI) has become increasingly prominent as contemporary oncology extends survival and intensifies combination regimens. Conventional chemotherapeutics, molecular targeted agents, immune checkpoint inhibitors, and immune cell-based therapies can induce distinct patterns of kidney injury, including proximal tubular toxicity with acute kidney injury, glomerular endothelial injury with proteinuria or thrombotic microangiopathy, immune-mediated acute interstitial nephritis, and systemic inflammatory or hemodynamic injury associated with cellular immunotherapy. Current management relies mainly on monitoring, supportive care, dose modification, and immunosuppression when indicated, yet these approaches are often reactive and may compromise anticancer treatment intensity. Therefore, effective strategies that preserve nephron structure and function without weakening antitumor efficacy remain an unmet need. Importantly, despite compelling biological rationale, no cell-based or cell-derived therapy has yet demonstrated improved long-term renal outcomes or overall survival in randomized trials involving cancer patients with ATRI. Cell-based and cell-derived therapies represent a promising direction for onco-nephroprotection by integrating immunomodulation, trophic support, and regenerative repair. Mesenchymal stem cells mainly act through paracrine programs to restrain inflammation, enhance tubular cell survival, and limit fibrotic remodeling, although limited renal delivery and oncologic safety remain major barriers. Renal progenitor and precursor cell strategies aim to promote structural repair but require strict control of cell purity, differentiation stage, and genomic stability. Exosomes are emerging as cell-free modalities, yet their cargo heterogeneity and context-dependent effects in tumor biology require careful evaluation. This mini review summarizes ATRI mechanisms, the rationale and evidence for major cellular platforms, and future directions for biomarker-guided translation.