Mitchinson M J
Med Hypotheses. 1983 Oct;12(2):171-8. doi: 10.1016/0306-9877(83)90079-8.
The suggestion has frequently been made that lipid-laden blood monocytes might contribute to atherosclerosis by emigrating into the arterial intima. In spite of much evidence that this occurs, the mechanism has never attracted widespread support as being of major importance, mainly because of the apparently small numbers of monocytes involved in this traffic, compared to the larger numbers of smooth muscle cells in the lesion. Recent observations suggest that some at least of the macrophages within the early lesion may be oxidising their lipid contents. Because some oxidised lipids are known to be toxic to cells, it is proposed that the production of oxidised lipids by macrophages may cause the death of these and other cells in the intima; and that-cell death begins the vicious circle of injury and further lipid accumulation which characterise the enlarging plaque.
人们经常提出这样的观点,即富含脂质的血液单核细胞可能通过迁移到动脉内膜而导致动脉粥样硬化。尽管有大量证据表明这种情况会发生,但该机制从未作为主要因素获得广泛支持,主要是因为与病变中数量较多的平滑肌细胞相比,参与这种迁移的单核细胞数量明显较少。最近的观察表明,早期病变内至少一些巨噬细胞可能正在氧化其脂质成分。由于已知一些氧化脂质对细胞有毒,因此有人提出巨噬细胞产生氧化脂质可能导致这些细胞和内膜中的其他细胞死亡;并且细胞死亡开启了损伤和进一步脂质积累的恶性循环,这是不断扩大的斑块的特征。