平滑肌细胞和基质金属蛋白酶作为动脉粥样硬化斑块稳定靶点的表型调节

G. Chaldakov, M. Zhelyazkova-Savova, Daniela Panayotova, M. Fiore, S. Yanev
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引用次数: 0

摘要

动脉粥样硬化及其并发症,斑块纤维帽的侵蚀和破裂,可导致心肌梗死和中风,这是全世界死亡的主要原因。在这种情况下,最内层介质的动脉平滑肌细胞(SMC)发生表型改变,转向分泌型表型,参与基质蛋白的产生。从本质上讲,这是一种保护作用,形成新的动脉层,即覆盖斑块血栓形成的脂质核心的纤维帽。斑块破裂的风险与纤维帽内分泌状态SMC和胶原原纤维的存在呈负相关。因此,纤维帽重塑似乎是斑块易感性的主要决定因素。在此,我们重点研究了(i)转录因子TCF21和KLF-4在SMC表型调节中的潜在作用,(ii) SMC基质蛋白分泌,以及(iii)蛋白酶(MMP, ADAM, ADAMTS, furin和MMP诱导剂CD147)在这一关键过程中的活性。我们认为,关注这些基本途径可能有助于了解纤维帽稳定性,这可能会转化为临床医学。
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Phenotypic modulation of smooth muscle cells and matrix metalloproteinases as targets for atherosclerotic plaque stabilization
Atherosclerosis and its complications, erosion and rupture of the plaque fibrous cap, lead to myocardial infarction and stroke, the main causes of mortality worldwide. In this setting, arterial smooth muscle cells (SMC) of the innermost media undergo phenotypic changes, a switch towards a secretory phenotype engaged in matrix proteins production. In its nature, this is a protective action that forms of a new arterial layer, the fibrous cap covering the plaque thrombogenic lipid core. The risk of plaque rupture is inversely correlated with the presence of secretory state SMC and collagen fibrils within the fibrous cap. Thus, fibrous cap remodeling appears to be the main determinant of plaque vulnerability. Herein, we focus on the potential role of (i) the transcription factors TCF21 and KLF-4 in SMC phenotypic modulation, (ii) the matrix protein secretion of SMC, and (iii) the activity of proteinases (MMP, ADAM, ADAMTS, furin, and the MMP inducer CD147) in this critical process. We argue that focusing on these basic pathways could contribute to the knowledge of fibrous cap stability that might be translated into clinical medicine.
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