Magle Stora Kyrkogata 9, Lund, Sweden.
Am J Med Sci. 2012 Nov;344(5):391-4. doi: 10.1097/MAJ.0b013e31824ba6e0.
There is a universal lack of exposure response between degree of lipid lowering and the outcome in clinical and angiographic trials questioning the current view on atherogenesis. However, there are numerous observations and experiments suggesting that microorganisms may play a causal role. A clue is the fact that the lipoproteins constitute an innate immune system by binding and inactivating microorganisms and their toxic products through formation of circulating complexes. Their size may increase in the presence of hyperhomocysteinemia because homocysteine reacts with low-density lipoprotein (LDL) to form homocysteinylated LDL aggregates. Autoantibodies against homocysteinylated or oxidized LDL may also enhance the aggregation. Because of the high extracapillary pressure, such aggregates may obstruct arterial vasa vasorum producing ischemia and cell death within the arterial wall leading to the creation of a vulnerable plaque. The many epidemiological observations, clinical findings and laboratory experiments that conflict with the cholesterol hypothesis are in good accordance with ours.
在临床和血管造影试验中，降脂程度与结果之间普遍缺乏相关性，这对动脉粥样硬化形成的现有观点提出了质疑。然而，有许多观察和实验表明，微生物可能起因果作用。一个线索是这样一个事实，即脂蛋白通过形成循环复合物来结合和失活微生物及其有毒产物，从而构成先天免疫系统。在高同型半胱氨酸血症的存在下，它们的大小可能会增加，因为同型半胱氨酸与低密度脂蛋白（LDL）反应形成同型半胱氨酸化 LDL 聚集体。针对同型半胱氨酸化或氧化 LDL 的自身抗体也可能增强聚集。由于毛细血管外压高，此类聚集体可能会阻塞血管腔，导致动脉壁内缺血和细胞死亡，从而产生易损斑块。与胆固醇假说相冲突的许多流行病学观察、临床发现和实验室实验与我们的观点非常一致。
