Belovici Maria Isabela, Pandele G I
Universitatea de Medicină şi Farmacie Gr.T. Popa Iaşi, Facultatea de Medicină, Clinica a VIa Medicală.
Rev Med Chir Soc Med Nat Iasi. 2008 Jan-Mar;112(1):21-34.
Arterial calcification was previously viewed as an inevitable, passive, and degenerative process that occurred at the end stages of atherosclerosis. Recent studies, however, have demonstrated that calcification of arteries is a complex and regulated process. It may occur in conjunction with atherosclerosis or in an isolated form that is commonly associated with diabetes and renal failure. Higher artery calcium scores are associated with increased cardiovascular events, and some aspects of arterial calcification are similar to the biology of forming bone. Arterial calcification can thus be viewed as a distinct inflammatory arteriopathy, much like atherosclerosis and aneurysms, with its own contribution to cardiovascular morbidity and mortality. Current research involves efforts to define the complex interactions between cellular and molecular mediators of arterial calcification and, in particular, the role of endogenous calcification inhibitors. This review discusses the clinical relevance, cellular events, and suspected molecular pathways that control arterial calcification.
动脉钙化曾被视为动脉粥样硬化末期不可避免的、被动的退行性过程。然而,最近的研究表明,动脉钙化是一个复杂且受调控的过程。它可能与动脉粥样硬化同时发生,或以一种通常与糖尿病和肾衰竭相关的孤立形式出现。较高的动脉钙评分与心血管事件增加相关,并且动脉钙化的某些方面类似于骨形成生物学。因此,动脉钙化可被视为一种独特的炎症性动脉病变,很像动脉粥样硬化和动脉瘤,对心血管发病率和死亡率有其自身的影响。当前的研究致力于确定动脉钙化的细胞和分子介质之间的复杂相互作用,特别是内源性钙化抑制剂的作用。本综述讨论了控制动脉钙化的临床相关性、细胞事件和疑似分子途径。