Analogous pathobiologic mechanisms in glomerulosclerosis and atherosclerosis.
Analogous pathobiologic mechanisms in glomerulosclerosis and atherosclerosis.
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发表时间：
1991-04
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通讯作者：
Jonathan R. Diamond
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作者：
Jonathan R. Diamond
本文试图进一步阐明动脉粥样硬化和肾小球硬化过程中所涉及的相似的病理生物学机制。特别是，最近的实验数据在这两个过程的模型集中在高胆固醇血症和单核细胞/巨噬细胞在传播这些病变的作用。在非免疫毒性肾小球病，慢性氨基糖苷类肾病，我们的实验室已经证明了一个重要的作用，肾小球巨噬细胞，这是增加的数量与蛋白尿的发病时间相关，在传播初始肾小球损伤肾小球硬化。此外，饮食性高胆固醇血症的叠加进一步增加了肾小球巨噬细胞的数量，并激活了全身巨噬细胞。这些数据表明，高胆固醇血症的肾病和激增的肾小球巨噬细胞数量在初始肾小球损伤后，在建立一个级联的细胞间的事件，最终在肾小球硬化症之间的协同作用。动脉粥样硬化血管壁中的脂肪条纹的演变和肾小球硬化的进行性肾小球病变之间的有趣的组织学和免疫组化相似性，提示类似的病理生物学机制。
This paper attempts to further delineate the similar pathobiologic mechanisms involved in the atherosclerosis and glomerulosclerosis processes. In particular, recent experimental data in models of both processes have focused on the roles of hypercholesterolemia and the monocyte/macrophage in propagating these lesions. In a nonimmune toxic glomerulopathy, chronic aminonucleoside nephrosis, our laboratory has demonstrated an important role for the glomerular macrophage, which is increased in number in temporal association with the onset of albuminuria, in propagating initial glomerular injury to glomerulosclerosis. In addition, a superimposition of dietary hypercholesterolemia further augments this heightened glomerular macrophage number and activates systemic macrophages. These data suggest a synergistic role between the hypercholesterolemia of nephrosis and the surge in glomerular macrophage number following initial glomerular injury in establishing a cascade of intercellular events that culminates in glomerulosclerosis. The intriguing histologic and immunohistochemical similarities between the evolving fatty streak in the atherosclerotic vessel wall and the progressive glomerular lesion leading to glomerulosclerosis suggest analogous pathobiologic mechanisms.