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近50年来随着人口老龄化程度的不断加深以及人们生活习惯的改变,退行性主动脉瓣疾病的发病率在全球范围内不断增加。该病是最常见的心脏瓣膜病,晚期主要表现为瓣膜钙化,其病理过程与动脉粥样硬化性血管疾病类似。到目前为止,引起主动脉瓣退行性变的分子机制还不是很清楚,但相关研究进展迅速。例如3-羟基-3-甲基戊二酰辅酶A还原酶抑制剂、血管紧张素转换酶、基质金属蛋白酶被众多学者认为是此类疾病的调节剂。参与瓣膜胚胎起源的信号因子Wnt,TGF-β1,BMP和Notch等也被认为参与了主动脉瓣的退行性改变。血管形成在该疾病中发挥重要作用。本文对退行性主动脉瓣疾病可能的分子致病机制进行综述,以期为进一步明确病因提供参考。
In the recent 50 years, with the deepening of the population aging and the change of people’s living habits, the incidence of degenerative aortic valve disease has been on a global scale. The disease is the most common valvular heart disease, the latter is mainly manifested as valve calcification, the pathological process and atherosclerotic vascular disease similar. So far, the molecular mechanism that causes aortic valve degeneration is not yet clear, but the relevant research is progressing rapidly. For example, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, angiotensin converting enzyme and matrix metalloproteinases are considered by many scholars as regulators of such diseases. Signaling factors Wnt, TGF-β1, BMP and Notch involved in the origin of valve embryos are also considered to be involved in degenerative changes in the aortic valve. Angiogenesis plays an important role in this disease. This article reviews the possible molecular pathogenesis of degenerative aortic valve disease in order to provide a reference for further clarifying the cause.