Proinflammation: the key to arterial aging.

Proinflammation: the key to arterial aging.
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DOI:
10.1016/j.tem.2013.10.002
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发表时间:
2014-02
影响因子:
10.9
通讯作者:
Lakatta, Edward G.
Lakatta, Edward G.
中科院分区:
医学1区
文献类型:
--
作者:
Wang, Mingyi;Jiang, Liqun;Monticone, Robert E.;Lakatta, Edward G.

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动脉老化是心血管疾病发病率和患病率增加的主要因素,这主要是由于慢性、低度、“无菌”动脉炎症的存在。由血管紧张素 II 级联驱动的炎症信号传导会导致与年龄相关的动脉结构和功能重塑。老化动脉的特征是内皮破坏、血管平滑肌细胞迁移和增殖增强、细胞外基质沉积、弹性蛋白断裂和基质钙化/淀粉样变性/糖化。重要的是,动脉老化的分子机制也与高血压和动脉粥样硬化的发病机制有关。与年龄相关的动脉促炎症在某种程度上是可变的,抑制或延迟它的干预措施可能有可能改善或延缓与年龄相关的动脉疾病。
Arterial aging is the major contributing factor to increases in the incidence and prevalence of cardiovascular disease, due mainly to the presence of chronic, low-grade, “sterile” arterial inflammation. Inflammatory signaling driven by the angiotensin II cascade perpetrates adverse age-associated arterial structural and functional remodeling. The aged artery is characterized by endothelial disruption, enhanced vascular smooth muscle cell migration and proliferation, extracellular matrix deposition, elastin fracture, and matrix calcification/amyloidosis/glycation. Importantly, the molecular mechanisms of arterial aging are also relevant to the pathogenesis of hypertension, and atherosclerosis. Age-associated arterial proinflammation is, to some extent, mutable, and interventions to suppress or delay it may have the potential to ameliorate or retard age-associated arterial diseases.
主动脉Calpain-1活性增加可介导与年龄相关的血管紧张素II信号的血管平滑肌细胞信号传导。
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