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首页> 外文期刊>Circulation journal >Balanced mineralization in the arterial system: Possible role of osteoclastogenesis/osteoblastogenesis in abdominal aortic aneurysm and stenotic disease
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Balanced mineralization in the arterial system: Possible role of osteoclastogenesis/osteoblastogenesis in abdominal aortic aneurysm and stenotic disease

机译：动脉系统中的矿物质平衡：破骨细胞生成/成骨细胞生成在腹主动脉瘤和狭窄疾病中的可能作用

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Arterial calcification is the result of the same highly organized processes as seen in bone, which rely on a delicate balance between osteoblasts and osteoclasts. Although previously understood as passive precipitation, evidence has accumulated to suggest that arterial calcification is the result of organized, regulated processes bearing many similarities to osteogenesis in bone, including the presence of subpopulations of arterial wall cells that retain osteoblastic lineage potential. These cells have the potential to form mineralized nodules and express osteoblast markers, including bone morphogenetic protein-2, osteocalcin, osteopontin, and alkaline phosphatase. By contrast, osteoclast-like cells mediate the catabolic process of mineral resorption. Recent data shows that cells positive for tartrate-re-sistant acid phosphatase, a major marker for osteoclasts, have been histologically identified in atherosclerotic lesions and are referred to as osteoclast-like cells. Evidence has accumulated to suggest that initial arterial calcification through passive precipitation of calcium phosphate initiates balanced mineralization regulated by osteoclast-like and osteoblast-like cells. Subsequently, various pathogenic conditions may trigger an imbalance between osteoblasto-genesis and osteoclastogenesis, leading to either calcification in stenotic/occlusive disease or destruction of the extracellular matrix in aneurysmal disease. Further elucidation of these newly emerging concepts could lead to a novel therapeutic approach to arterial stenotic/occlusive disease and/or abdominal aortic aneurysm.
机译：动脉钙化是与骨骼中相同的高度组织化过程的结果，该过程依赖于成骨细胞和破骨细胞之间的微妙平衡。尽管先前被理解为被动沉淀，但已有证据表明动脉钙化是组织化，受调节的过程的结果，该过程与骨骼中的成骨作用具有许多相似之处，包括存在保留成骨细胞谱系潜力的动脉壁细胞亚群。这些细胞有可能形成矿化的结节并表达成骨细胞标志物，包括骨形态发生蛋白2，骨钙素，骨桥蛋白和碱性磷酸酶。相反，破骨细胞样细胞介导矿物质吸收的分解代谢过程。最近的数据显示，在动脉粥样硬化病变中已在组织学上鉴定了酒石酸抗性酸性磷酸酶（破骨细胞的主要标志物）呈阳性的细胞，被称为破骨细胞样细胞。已有证据表明，通过磷酸钙的被动沉淀引起的初始动脉钙化可启动由破骨细胞样和成骨细胞样细胞调节的平衡矿化作用。随后，各种致病条件可能触发成骨细胞生成与破骨细胞生成之间的失衡，从而导致狭窄/闭塞性疾病中的钙化或动脉瘤性疾病中细胞外基质的破坏。这些新出现的概念的进一步阐明可能会导致一种针对动脉狭窄/闭塞性疾病和/或腹主动脉瘤的新颖治疗方法。

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