BIOLOGICAL AND BIOCHEMICAL-PROPERTIES OF FIBROBLAST GROWTH-FACTORS - IMPLICATIONS FOR THE PATHOGENESIS OF ATHEROSCLEROSIS
BIOLOGICAL AND BIOCHEMICAL-PROPERTIES OF FIBROBLAST GROWTH-FACTORS - IMPLICATIONS FOR THE PATHOGENESIS OF ATHEROSCLEROSIS
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DOI：
10.1161/01.atv.9.3.269
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发表时间：
1989-05-01
期刊：
影响因子：
--
通讯作者：
EDELMAN, ER
中科院分区：
文献类型：
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作者：
KLAGSBRUN, M;EDELMAN, ER
动脉粥样硬化一词最初是由Thoma于1886年创造的，旨在描述一种涉及血管壁进行性硬化的退行性过程。[1]今天，我们已经进一步认识到，最终的动脉粥样硬化病变是一个复杂的和异质性的快速增殖和迁移的细胞，产生和支持一个活跃的结缔组织基质的安排。动脉粥样硬化病变有两种主要形式：脂肪条纹和纤维斑块。典型的脂肪条纹是沿血流方向延伸的凸起、狭窄、发黄的病变。它们是非梗阻性的，可能是更晚期病变的前兆，但尚未证实。条纹的特征是泡沫细胞、平滑肌细胞（SMC）、T淋巴细胞和脂质、胶原蛋白、弹性蛋白和蛋白聚糖的细胞外基质的内皮下集合。2-3-4单克隆抗体研究表明，泡沫细胞主要是单核细胞衍生的巨噬细胞，偶尔是吸收了胆固醇和胆固醇酯的SMC。5纤维斑块是晚期动脉粥样硬化的基本和特征性病变。这种病变的组织学组成是可变的，但通常由细胞碎片、脂质、胆固醇和钙沉积物的坏死核心组成，其上覆盖有SMC、巨噬细胞和T淋巴细胞，所有这些都被一层由SMC、白细胞和致密结缔组织基质组成的纤维组织覆盖。图8较大的斑块被从外膜上升起的血管所包围。7随着疾病的进展，斑块可能进一步退化，包括钙化、溃疡和坏死。如此复杂的病变容易发生壁内出血-
The term, atherosclerosis, as it was originally coined by Thoma in 1886, was devised to describe a degenerative process involving the progressive hardening of the blood vessel wall. 1 Today we have advanced to the understanding that the ultimate atherosclerotic lesion is a complex and heterogeneous arrangement of rapidly proliferating and migrating cells that produce and support an active connective tissue matrix. Two major forms of atherosclerotic lesions have been described: the fatty streak and the fibrous plaque. Classic fatty streaks are raised, narrow, yellowed lesions that extend in the direction of blood flow. They are nonobstructive and are likely, but yet unproven, precursors of more advanced lesions. The streaks are characterized by subendothelial collections of foam cells, smooth muscle cells (SMC), T-lymphocytes, and an extracellular matrix of lipid, collagen, elastin, and proteoglycan. 2-3-4 Monoclonal antibody studies have shown that foam cells are primarily monocyte-derived macrophages and occasionally SMC that have imbibed cholesterol and cholesterol esters. 5The fundamental and characteristic lesion of advanced atherosclerosis is the fibrous plaque. The histobgical composition of this lesion is variable but typically consists of a necrotic core of cellular debris, lipid, cholesterol, and calcium deposits overlain by SMC, macrophages, and T-lymphocytes, all of which are capped by a layer of fibrous tissue that is composed of SMC, leukocytes, and a dense connective tissue matrix. 8 Larger plaques are surrounded by a vasa vasorum that rises from the adventitia. 7 As disease advances, plaque may undergo further degeneration, including calcification, ulceration, and necrosis. Such complicated lesions are prone to intramural hemor-