Siennicka Aldona, Zapolska-Downar Danuta
Katedra Biochemii Klinicznej i Diagnostyki Laboratoryjnej, Pomorskiej Akademii Medycznej w Szczecinie.
Postepy Hig Med Dosw. 2003;57(2):219-37.
The precise mechanisms of LDL oxidation in vivo are not well-known but the presence of several enzymes and agents capable of modifying LDL particles was noted in arterial wall. These reactive agents modify lipid, protein as well as antioxidant component of the LDL particles. Postsecretory modification in LDL structure trigger its atherogenic potential. LDL particles retained in the artery wall interact with the various forms of proteoglycans in the extracellular matrix, that increases the resident time of LDL in endothelial space and allows extensive modification. The modified forms of LDL are able to activate intimal cells and to trigger various inflammatory signals. In turn, activated intimal cells can secrete enzymes and agents capable of modifying LDL. These processes can initiate and maintain a vicious circle in the intima and lead to lesion progression.
低密度脂蛋白（LDL）在体内氧化的确切机制尚不清楚，但在动脉壁中发现了几种能够修饰LDL颗粒的酶和物质。这些反应性物质会修饰LDL颗粒的脂质、蛋白质以及抗氧化成分。LDL结构的分泌后修饰引发其致动脉粥样硬化潜力。滞留在动脉壁中的LDL颗粒与细胞外基质中各种形式的蛋白聚糖相互作用，这增加了LDL在内皮空间的驻留时间并允许广泛修饰。修饰后的LDL形式能够激活内膜细胞并触发各种炎症信号。反过来，活化的内膜细胞可以分泌能够修饰LDL的酶和物质。这些过程可以在内膜中引发并维持恶性循环，导致病变进展。
