Department of Cardiology, The People's Hospital of Guangxi Zhuang Autonomous Region and Research Center of Cardiovascular Disease, Guangxi Academy of Medical Sciences, Nanning, China.
Department of Cardiology, The First Affiliated Hospital of Guangxi Medical University and Guangxi Key Laboratory Base of Precision Medicine in Cardiocerebrovascular Diseases Control and Prevention and Guangxi Clinical Research Center for Cardiocerebrovascular Diseases, Nanning, China.
Int Urol Nephrol. 2024 Jul;56(7):2291-2299. doi: 10.1007/s11255-024-03981-2. Epub 2024 Mar 5.
Percutaneous coronary intervention (PCI) is a crucial diagnostic and therapeutic approach for coronary heart disease. Contrast agents' exposure during PCI is associated with a risk of contrast-induced acute kidney injury (CI-AKI). CI-AKI is characterized by a sudden decline in renal function occurring as a result of exposure to intravascular contrast agents, which is associated with an increased risk of poor prognosis. The pathophysiological mechanisms underlying CI-AKI involve renal medullary hypoxia, direct cytotoxic effects, endoplasmic reticulum stress, inflammation, oxidative stress, and apoptosis. To date, there is no effective therapy for CI-AKI. High-mobility group box 1 (HMGB1), as a damage-associated molecular pattern molecule, is released extracellularly by damaged cells or activated immune cells and binds to related receptors, including toll-like receptors and receptor for advanced glycation end product. In renal injury, HMGB1 is expressed in renal tubular epithelial cells, macrophages, endothelial cells, and glomerular cells, involved in the pathogenesis of various kidney diseases by activating its receptors. Therefore, this review provides a theoretical basis for HMGB1 as a therapeutic intervention target for CI-AKI.
经皮冠状动脉介入治疗（PCI）是冠心病的重要诊断和治疗方法。PCI 期间造影剂的暴露与造影剂引起的急性肾损伤（CI-AKI）的风险相关。CI-AKI 的特征是由于暴露于血管内造影剂而导致肾功能突然下降，这与预后不良的风险增加有关。CI-AKI 的病理生理机制涉及肾髓质缺氧、直接细胞毒性作用、内质网应激、炎症、氧化应激和细胞凋亡。迄今为止，CI-AKI 尚无有效的治疗方法。高迁移率族蛋白 B1（HMGB1）作为损伤相关分子模式分子，由受损细胞或激活的免疫细胞释放到细胞外，并与相关受体（包括 Toll 样受体和晚期糖基化终产物受体）结合。在肾损伤中，HMGB1 在肾小管上皮细胞、巨噬细胞、内皮细胞和肾小球细胞中表达，通过激活其受体参与各种肾脏疾病的发病机制。因此，本综述为 HMGB1 作为 CI-AKI 的治疗干预靶点提供了理论依据。
