Major factors leading to the development of atherosclerosis are a high cholesterol (Chol) level in the blood and oxidative stress. Both promote the formation of Chol microcrystals in blood vessel walls. Deposition of Chol microcrystals in arterial intima causes inflammation, which initiates and accompanies the atherosclerotic process in all its phases. One of the possible sources of Chol in the blood vessel walls is oxidized low-density lipoproteins—this atherosclerotic plaque formation pathway has already been described in the literature. Here, we hypothesize that initiation of the atherosclerotic process may involve Chol domains in the plasma membranes of arterial cells. Increased Chol content and the presence of polyunsaturated phospholipids in these membranes together with oxidative stress (phospholipid peroxidation) may lead to the formation of pure Chol bilayer domains that, with further peroxidation and increased Chol content, may collapse in the form of Chol seed crystals. Independent of their origin, Chol microcrystals activate inflammasomes, thereby stimulate immune responses, and initiate inflammation that may lead to the development of atherosclerosis. This new, hypothetical pathway has not yet been investigated in depth; however, data from the literature and our own results support its feasibility.

中文翻译：

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胆固醇微晶形成引发动脉粥样硬化过程的假想途径。

导致动脉粥样硬化发展的主要因素是血液中的高胆固醇 (Chol) 水平和氧化应激。两者都促进血管壁中 Chol 微晶的形成。Chol 微晶在动脉内膜中的沉积引起炎症，炎症引发并伴随动脉粥样硬化过程的所有阶段。血管壁中 Chol 的可能来源之一是氧化的低密度脂蛋白——文献中已经描述了这种动脉粥样硬化斑块形成途径。在这里，我们假设动脉粥样硬化过程的启动可能涉及动脉细胞质膜中的 Chol 结构域。这些膜中 Chol 含量的增加和多不饱和磷脂的存在以及氧化应激（磷脂过氧化）可能导致纯 Chol 双层结构域的形成，随着进一步的过氧化和 Chol 含量的增加，可能以 Chol 晶种的形式坍塌。独立于它们的来源，Chol 微晶激活炎性体，从而刺激免疫反应，并引发可能导致动脉粥样硬化发展的炎症。这种新的假设途径尚未得到深入研究；然而，来自文献的数据和我们自己的结果支持其可行性。从而刺激免疫反应，并引发可能导致动脉粥样硬化发展的炎症。这种新的假设途径尚未得到深入研究；然而，来自文献的数据和我们自己的结果支持其可行性。从而刺激免疫反应，并引发可能导致动脉粥样硬化发展的炎症。这种新的假设途径尚未得到深入研究；然而，来自文献的数据和我们自己的结果支持其可行性。