The aging population is increasing dramatically. Aging-associated stress simultaneously drives proinflammatory remodeling, involving angiotensin II and other factors, in both the heart and large arteries. The structural remodeling and functional changes that occur with aging include cardiac and vascular wall stiffening, systolic hypertension and suboptimal ventricular-arterial coupling, features that are often clinically silent and thus termed a silent syndrome. These age-related effects are the result of responses initiated by cardiovascular proinflammatory cells. Local proinflammatory signals are coupled between the heart and arteries due to common mechanical and humoral messengers within a closed circulating system. Thus, targeting proinflammatory signaling molecules would be a promising approach to improve age-associated suboptimal ventricular-arterial coupling, a major predisposing factor for the pathogenesis of clinical cardiovascular events such as heart failure.

中文翻译：

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心脏和大动脉中与年龄相关的促炎重塑和功能表型。

人口老龄化正在急剧增加。与衰老相关的压力同时推动了心脏和大动脉中的促炎性重塑，包括血管紧张素 II 和其他因素。随着衰老发生的结构重塑和功能变化包括心脏和血管壁僵硬、收缩期高血压和心室-动脉耦合欠佳，这些特征通常在临床上是无声的，因此被称为无声综合征。这些与年龄相关的影响是心血管促炎细胞引发的反应的结果。由于封闭循环系统中常见的机械和体液信使，局部促炎信号在心脏和动脉之间耦合。因此，