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肺移植的长期成功率受到慢性移植物功能障碍的限制,而慢性移植物功能障碍主要原因是闭塞性细支气管炎(OB)。OB形成的病理机制涉及异常的呼吸道上皮重塑、血管重塑、基质重塑和淋巴系统新生。一个潜在的机制是损伤和异常重塑的恶性循环,导致OB不断加重。也就是说,解剖和功能的异常(如上皮重塑减弱黏膜纤毛清除能力,加重误吸相关的损伤)诱导和恶化免疫介导和非免疫介导通路。本文综述了OB发生的病理机制和药物治疗的新进展。
The long-term success rate of lung transplantation is limited by chronic graft dysfunction, whereas the main cause of chronic graft dysfunction is obliterative bronchiolitis (OB). The pathophysiology of OB formation involves abnormal remodeling of the respiratory epithelium, remodeling of blood vessels, stromal remodeling, and neoplasia of the lymphatic system. A potential mechanism is the vicious cycle of injury and abnormal remodeling that causes the OB to worsen. That is, abnormalities in anatomy and function (such as epithelial remodeling impair mucociliary clearance, aggravate aspiration-related damage) induce and worsen immune-mediated and non-immune mediated pathways. This article reviews the pathogenesis of OB and the new progress of drug treatment.