Mechanisms of pathologic calcification.
Mechanisms of pathologic calcification.
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发表时间：
1988
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通讯作者：
H. Anderson
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作者：
H. Anderson
病理性钙化通常由线粒体或基质囊泡的生物膜引起。线粒体经常引发细胞内钙化。通过出芽或细胞破裂从细胞外膜衍生的基质囊泡在钙化性肌腱炎、磷灰石沉积性骨关节炎、动脉粥样硬化、心脏瓣膜钙化、鼓膜炎和其他钙化性疾病中引发细胞外钙化。基质囊泡和线粒体通常通过磷酸酶与钙结合磷脂（两者都是膜结合的）的相互作用启动钙化。羟基磷灰石（HA）晶体首先在膜封闭的微空间的保护性微环境内形成。一旦形成并暴露于细胞外液，HA晶体可以作为细胞核或模板，从而支持渐进的自催化矿物晶体增殖。
Pathologic calcification usually is initiated by the biologic membranes of mitochondria or matrix vesicles. Mitochondria frequently initiate intracellular calcification. Matrix vesicles, derived from the outer membrane of cells by budding or cell disruption, initiate extracellular calcification in calcific tendonitis, apatite-deposition osteoarthritis, atherosclerosis, cardiac valvular calcification, tympanosclerosis, and other calcific diseases. Matrix vesicles and mitochondria usually initiate calcification through the interaction of phosphatase enzymes with calcium-binding phospholipids, both of which are membrane-bound. Hydroxyapatite (HA) crystals are formed first within the protective microenvironment of the membrane-enclosed microspace. Once formed and exposed to the extracellular fluid, HA crystals can serve as nuclei or templates, thus supporting progressive, autocatalytic mineral crystal proliferation.