Tabas Ira, García-Cardeña Guillermo, Owens Gary K
Department of Medicine, Department of Pathology and Cell Biology, and Department of Physiology, Columbia University Medical Center, New York, NY 10032 Department of Medicine, Department of Pathology and Cell Biology, and Department of Physiology, Columbia University Medical Center, New York, NY 10032 Department of Medicine, Department of Pathology and Cell Biology, and Department of Physiology, Columbia University Medical Center, New York, NY 10032
Program in Human Biology and Translational Medicine, Harvard Medical School, Boston, MA 02115 Center for Excellence in Vascular Biology, Department of Pathology, Brigham and Women's Hospital, Boston, MA 02115.
J Cell Biol. 2015 Apr 13;209(1):13-22. doi: 10.1083/jcb.201412052.
Atherosclerosis occurs in the subendothelial space (intima) of medium-sized arteries at regions of disturbed blood flow and is triggered by an interplay between endothelial dysfunction and subendothelial lipoprotein retention. Over time, this process stimulates a nonresolving inflammatory response that can cause intimal destruction, arterial thrombosis, and end-organ ischemia. Recent advances highlight important cell biological atherogenic processes, including mechanotransduction and inflammatory processes in endothelial cells, origins and contributions of lesional macrophages, and origins and phenotypic switching of lesional smooth muscle cells. These advances illustrate how in-depth mechanistic knowledge of the cellular pathobiology of atherosclerosis can lead to new ideas for therapy.
动脉粥样硬化发生在中动脉的内皮下间隙（内膜）中血流紊乱的区域，由内皮功能障碍和内皮下脂蛋白潴留之间的相互作用引发。随着时间的推移，这个过程会激发一种无法消退的炎症反应，从而导致内膜破坏、动脉血栓形成和终末器官缺血。最近的进展突出了重要的细胞生物学致动脉粥样硬化过程，包括内皮细胞中的机械转导和炎症过程、损伤巨噬细胞的起源和作用，以及损伤平滑肌细胞的起源和表型转换。这些进展说明了对动脉粥样硬化细胞病理生物学的深入机制性认识如何能够带来新的治疗思路。
