文献类型：期刊文献

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

作者：Tian P.; Hu R.; Xue M.; Liang J.; Li J.; Li J.

第一作者：Tian P.

机构：[1]Clinical College of Traditional Chinese Medicine, Gansu University of Chinese Medicine, Lanzhou, China

第一机构：甘肃中医药大学

年份：2026

卷号：19

起止页码：1

外文期刊名：Journal of Inflammation Research

收录：Scopus(收录号：2-s2.0-105029122716)

语种：英文

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

摘要：Acute kidney injury (AKI) is a common and serious dose-limiting complication of cisplatin chemotherapy. Cisplatin-induced 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-κB) 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-κB 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. ? 2026 Tian et al.