Department of Biomedical Engineering, Vascular Biology and Therapeutics Program, Yale University, New Haven, Connecticut, USA.
Am J Hypertens. 2021 May 22;34(5):432-441. doi: 10.1093/ajh/hpaa195.
Hypertension is both a cause and a consequence of central artery stiffening, which in turn is an initiator and indicator of myriad disease conditions and thus all-cause mortality. Such stiffening results from a remodeling of the arterial wall that is driven by mechanical stimuli and mediated by inflammatory signals, which together lead to differential gene expression and concomitant changes in extracellular matrix composition and organization. This review focuses on biomechanical mechanisms by which central arteries remodel in hypertension within the context of homeostasis-what promotes it, what prevents it. It is suggested that the vasoactive capacity of the wall and inflammatory burden strongly influence the ability of homeostatic mechanisms to adapt the arterial wall to high blood pressure or not. Maladaptation, often reflected by inflammation-driven adventitial fibrosis, not just excessive intimal-medial thickening, significantly diminishes central artery function and disturbs hemodynamics, ultimately compromising end organ perfusion and thus driving the associated morbidity and mortality. It is thus suggested that there is a need for increased attention to controlling both smooth muscle phenotype and inflammation in hypertensive remodeling of central arteries, with future studies of the often adaptive response of medium-sized muscular arteries promising to provide additional guidance.
高血压既是中央动脉僵硬的原因，也是其后果，而中央动脉僵硬又是无数疾病状况的启动因素和指标，因此也是全因死亡率的指标。这种僵硬是由动脉壁的重塑引起的，其由机械刺激驱动，并由炎症信号介导，这些共同导致了差异基因表达以及细胞外基质组成和组织的相应变化。这篇综述主要关注高血压中中央动脉在稳态下重塑的生物力学机制——促进重塑的因素，防止重塑的因素。有人认为，血管壁的血管活性和炎症负担强烈影响着稳态机制适应高血压的能力。适应性差，通常表现为炎症驱动的外膜纤维化，而不仅仅是内膜中层过度增厚，显著降低了中央动脉的功能并扰乱了血液动力学，最终损害了终末器官的灌注，从而导致相关的发病率和死亡率。因此，有人建议，需要更加关注控制高血压时中央动脉中平滑肌表型和炎症，对中型肌性动脉的适应性反应的进一步研究有望提供更多的指导。
