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已发表论文
炎症：顺铂诱导肾损伤的病理轴线
Authors Tian P, Hu R, Xue M, Liang J , Li J, Li J
Received 15 August 2025
Accepted for publication 13 January 2026
Published 30 January 2026 Volume 2026:19 557661
DOI https://doi.org/10.2147/JIR.S557661
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Wenjian Li
Ping Tian, Rong Hu, MeiHao Xue, JianQing Liang, JinTian Li, Juan Li
Clinical College of Traditional Chinese Medicine, Gansu University of Chinese Medicine, Lanzhou, People’s Republic of China
Correspondence: JinTian Li, Clinical College of Traditional Chinese Medicine, Gansu University of Chinese Medicine, Lanzhou, 730000, People’s Republic of China, Email sh15294181882@163.com Juan Li, Clinical College of Traditional Chinese Medicine, Gansu University of Chinese Medicine, Lanzhou, 730000, People’s Republic of China, Email whnviphome@163.com
Abstract: 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.
Keywords: cisplatin, AKI, RTECs, macrophages, inflammation
Clinical College of Traditional Chinese Medicine, Gansu University of Chinese Medicine, Lanzhou, People’s Republic of China
Correspondence: JinTian Li, Clinical College of Traditional Chinese Medicine, Gansu University of Chinese Medicine, Lanzhou, 730000, People’s Republic of China, Email sh15294181882@163.com Juan Li, Clinical College of Traditional Chinese Medicine, Gansu University of Chinese Medicine, Lanzhou, 730000, People’s Republic of China, Email whnviphome@163.com
Abstract: 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.
Keywords: cisplatin, AKI, RTECs, macrophages, inflammation