Bonventre Joseph V, Zuk Anna
Medical Services, Brigham and Women's Hospital and Department of Medicine, Harvard Medical School, and Harvard-Massachusetts Institute of Technology, Division of Health Sciences and Technology, Charlestown, USA.
Kidney Int. 2004 Aug;66(2):480-5. doi: 10.1111/j.1523-1755.2004.761_2.x.
Inflammation plays a major role in the pathophysiology of acute renal failure resulting from ischemia. In this review, we discuss the contribution of endothelial and epithelial cells and leukocytes to this inflammatory response. The roles of cytokines/chemokines in the injury and recovery phase are reviewed. The ability of the mouse kidney to be protected by prior exposure to ischemia or urinary tract obstruction is discussed as a potential model to emulate as we search for pharmacologic agents that will serve to protect the kidney against injury. Understanding the inflammatory response prevalent in ischemic kidney injury will facilitate identification of molecular targets for therapeutic intervention.
炎症在缺血所致急性肾衰竭的病理生理学中起主要作用。在本综述中,我们讨论了内皮细胞、上皮细胞和白细胞在这种炎症反应中的作用。对细胞因子/趋化因子在损伤和恢复阶段的作用进行了综述。探讨了小鼠肾脏通过预先暴露于缺血或尿路梗阻而得到保护的能力,作为一种潜在模型,以便在我们寻找能保护肾脏免受损伤的药物时进行模仿。了解缺血性肾损伤中普遍存在的炎症反应将有助于确定治疗干预的分子靶点。