Kim K M
Department of Pathology, V. A. Medical Center and LSU Medical Center, Shreveport, Louisiana 71101-4295, USA.
Scanning Microsc. 1995;9(4):1137-75; discussion 1175-8.
Calcification in necrosis has long been known. Of the tissue components, the cells are most vulnerable. Nevertheless, little attention has been paid to the role of cell death in calcification. This review attempts to update the mechanism of calcification with an emphasis on the role of apoptosis in calcification. A brief review on the basic sciences relevant to calcification is followed by a discussion of abnormal Ca2+ and Pi homeostasis in cell injury and apoptosis. Concomitant increases in Ca2+ and Pi in blebs (and matrix vesicles) formed by apoptotic and/or necrotic cells are apparently the primary mechanism of calcification. In addition, membranous cellular degradation products (CDP) resulting from cell disintegration in toto frequently serve as the nidus of calcification. Published data on physiological calcification are compared with findings in various dystrophic calcinoses. This led to the conclusion that apoptosis most likely underlies the mechanism of both physiological and pathological calcifications. It is concluded that calcification is an important function of apoptosis. The mechanism of calcification by CDP and morphology of the resultant calcific deposits are complex.
坏死中的钙化早已为人所知。在组织成分中,细胞最为脆弱。然而,细胞死亡在钙化中的作用却很少受到关注。本综述试图更新钙化机制,重点关注凋亡在钙化中的作用。在简要回顾与钙化相关的基础科学之后,讨论细胞损伤和凋亡中异常的Ca2+和Pi稳态。凋亡和/或坏死细胞形成的小泡(和基质小泡)中Ca2+和Pi的同时增加显然是钙化的主要机制。此外,细胞整体崩解产生的膜性细胞降解产物(CDP)常常充当钙化的核心。将已发表的关于生理性钙化的数据与各种营养不良性钙化的研究结果进行比较。由此得出结论,凋亡很可能是生理性和病理性钙化机制的基础。得出的结论是,钙化是凋亡的一项重要功能。CDP导致钙化的机制以及由此产生的钙化沉积物的形态很复杂。