Division of Nephrology, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-8856, USA.
Pediatr Nephrol. 2012 Oct;27(10):1847-54. doi: 10.1007/s00467-011-2029-0. Epub 2011 Oct 28.
Ischemic acute kidney injury (AKI) contributes to considerable morbidity and mortality in hospitalized patients and can contribute to rejection during kidney transplantation. Maladaptive immune responses can exacerbate injury, and targeting these responses holds promise as therapy for AKI. In the last decade, a number of molecules and receptors were identified in the innate immune response to ischemia-reperfusion injury. This review primarily focuses on one pathway that leads to maladaptive inflammation: toll-like receptor 4 (TLR4) and one of its ligands, high mobility group box protein 1 (HMGB1). The temporal-spatial roles and potential therapeutics targeting this particular receptor-ligand interaction are also explored.
缺血性急性肾损伤（AKI）可导致住院患者出现较高的发病率和死亡率，并可导致肾移植过程中的排斥反应。适应性免疫反应可加重损伤，针对这些反应作为 AKI 的治疗方法具有一定的应用前景。在过去十年中，在缺血再灌注损伤的固有免疫反应中已经鉴定出许多分子和受体。本综述主要关注导致适应性炎症的一条途径： Toll 样受体 4（TLR4）及其配体之一，高迁移率族蛋白 B1（HMGB1）。还探讨了该特定受体-配体相互作用的时空作用和潜在的治疗方法。
