文献类型：期刊文献

英文题名：Inflammation: The Pathological Axis of Cisplatin-Induced Renal Injury

作者：Tian, Ping[1];Hu, Rong[1];Xue, Meihao[1];Liang, Jianqing[1];Li, Jintian[1,2];Li, Juan[1,2]

第一作者：Tian, Ping

通信作者：Li, JT[1];Li, J[1];Li, JT[2];Li, J[2]

机构：[1]Gansu Univ Chinese Med, Clin Coll Tradit Chinese Med, Lanzhou, Peoples R China;[2]Gansu Univ Chinese Med, Clin Coll Tradit Chinese Med, Lanzhou 730000, Peoples R China

第一机构：甘肃中医药大学中医临床学院

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Clin Coll Tradit Chinese Med, Lanzhou, Peoples R China;[2]corresponding author), Gansu Univ Chinese Med, Clin Coll Tradit Chinese Med, Lanzhou 730000, Peoples R China.|[10735ccd4a8840d96ab71]甘肃中医药大学中医临床学院;[10735]甘肃中医药大学;

年份：2026

卷号：19

起止页码：1.0

外文期刊名：JOURNAL OF INFLAMMATION RESEARCH

收录：;WOS:【SCI-EXPANDED(收录号:WOS:001693073000001)】；

基金："Double First-class" Key Scientific Research Project of Gansu Province in 2021 (GSSYLXM-05); Supported by National Natural Science Foundation of China in 2021, (No. 82160872); Major Cultivation Project of University Scientific Research Innovation Platform in 2024 (2024CXPT-08); Graduate Innovation Star Project of Gansu Province (2025CXZX-913).

语种：英文

外文关键词：cisplatin; AKI; RTECs; macrophages; inflammation

摘要：Acute kidney injury (AKI) is a common and serious dose-limiting complication of cisplatin chemotherapy. Cisplatininduced AKI (CI-AKI) is initiated predominantly in proximal renal tubular epithelial cells (RTECs), where cisplatin enters through organic cation transporter 2 (OCT2) and copper transporter 1 (CTR1). This accumulation drives mitochondrial dysfunction, reactive oxygen species (ROS) overproduction, and the release of damage-associated molecular patterns (DAMPs). These signals activate key innate immune pathways, including Toll-like receptor 4/myeloid differentiation primary response 88/nuclear factor kappa B (TLR4/ MyD88/NF-kappa B) signaling and the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, leading to a cytokine-driven inflammatory response. Macrophages are major infiltrating immune cells in CI-AKI: early M1 polarization amplifies tubular damage, whereas later M2-like macrophages support inflammation resolution and tissue repair. This review summarizes the mechanistic links between RTEC injury, innate immune activation, and RTEC-macrophage crosstalk, and highlights therapeutic opportunities such as TLR4/NF-kappa B blockade and modulation of macrophage polarization to reduce nephrotoxicity without compromising anticancer efficacy. Overall, an inflammation-centered view of RTEC-macrophage interactions may guide the development of effective renoprotective adjuncts for cisplatin-based regimens.