Reznichenko Anna, Korstanje Ron
Jackson Laboratory, Bar Harbor, Maine.
Jackson Laboratory, Bar Harbor, Maine.
Am J Pathol. 2015 Apr;185(4):888-96. doi: 10.1016/j.ajpath.2014.11.025. Epub 2015 Feb 2.
Platelet-activating factor (PAF) is a powerful proinflammatory mediator that displays an exceedingly diverse spectrum of biological effects. Importantly, PAF is shown to participate in a broad range of pathologic conditions. This review focuses on the role that PAF plays specifically in the pathophysiology of the kidney, the organ that is both a source and a target of PAF. Renal mesangial cells are responsible for glomerular PAF generation and, ultimately, are the victims of its excessive production. Mesangial pathology is widely acknowledged to reflect glomerular damage, which culminates in glomerulosclerosis and proteinuria. Therefore, modulation of mesangial cell responses would offer a pathophysiology-based therapeutic approach to prevent glomerular injury. However, the currently available therapeutic modalities do not allow for targeted intervention into these processes. A more profound understanding of the mechanisms that govern PAF metabolism and signaling in mesangial cells is important, because it could facilitate the quest for improved therapies for renal patients on the basis of PAF as a drug target.
血小板活化因子（PAF）是一种强大的促炎介质，具有极其多样的生物学效应。重要的是，PAF已被证明参与多种病理状况。本综述聚焦于PAF在肾脏病理生理学中所起的特定作用，肾脏既是PAF的来源又是其作用靶点。肾系膜细胞负责肾小球PAF的产生，最终也是PAF过量产生的受害者。系膜病变被广泛认为反映了肾小球损伤，最终导致肾小球硬化和蛋白尿。因此，调节系膜细胞反应将提供一种基于病理生理学的治疗方法来预防肾小球损伤。然而，目前可用的治疗方式无法对这些过程进行靶向干预。更深入了解调控系膜细胞中PAF代谢和信号传导的机制很重要，因为这有助于寻求以PAF作为药物靶点来改善肾病患者的治疗方法。
