Center for Molecular and Cellular Biology of Inflammation (CMCBI), Division of Immunology, Infection and Inflammatory Diseases (DIIID), Guys Campus, London SE1 1UL, UK.
Nat Rev Cardiol. 2010 Feb;7(2):77-86. doi: 10.1038/nrcardio.2009.228. Epub 2010 Jan 12.
Chronic inflammation drives atherosclerosis, the leading cause of cardiovascular disease. Over the past two decades, data have emerged showing that immune cells are involved in the pathogenesis of atherosclerotic plaques. The accumulation and continued recruitment of leukocytes are associated with the development of 'vulnerable' plaques. These plaques are prone to rupture, leading to thrombosis, myocardial infarction or stroke, all of which are frequent causes of death. Plaque macrophages account for the majority of leukocytes in plaques, and are believed to differentiate from monocytes recruited from circulating blood. However, monocytes represent a heterogenous circulating population of cells. Experiments are needed to address whether monocyte recruitment to plaques and effector functions, such as the formation of foam cells, the production of nitric oxide and reactive oxygen species, and proteolysis are critical for the development and rupture of plaques, and thus for the pathophysiology of atherosclerosis, as well as elucidate the precise mechanisms involved.
慢性炎症会导致动脉粥样硬化,这是心血管疾病的主要病因。在过去的二十年中,有数据表明免疫细胞参与了动脉粥样硬化斑块的发病机制。白细胞的积累和持续募集与“易损”斑块的发展有关。这些斑块容易破裂,导致血栓形成、心肌梗死或中风,这些都是导致死亡的常见原因。斑块中的巨噬细胞占斑块中白细胞的大部分,据信它们是从循环血液中募集而来的单核细胞分化而来的。然而,单核细胞是一个异质性的循环细胞群体。需要进行实验来确定单核细胞向斑块的募集及其效应功能(如泡沫细胞的形成、一氧化氮和活性氧的产生以及蛋白水解)是否对斑块的发展和破裂,以及动脉粥样硬化的病理生理学至关重要,并阐明涉及的精确机制。