Arteries are exposed to relentless pulsatile haemodynamic loads, but via mechanical homeostasis they tend to maintain near optimal structure, properties and function over long periods in maturity in health. Numerous insults can compromise such homeostatic tendencies, however, resulting in maladaptations or disease. Chronic inflammation can be counted among the detrimental insults experienced by arteries, yet inflammation can also play important homeostatic roles. In this paper, we present a new theoretical model of complementary mechanobiological and immunobiological control of vascular geometry and composition, and thus properties and function. We motivate and illustrate the model using data for aortic remodelling in a common mouse model of induced hypertension. Predictions match the available data well, noting a need for increased data for further parameter refinement. The overall approach and conclusions are general, however, and help to unify two previously disparate literatures, thus leading to deeper insight into the separate and overlapping roles of mechanobiology and immunobiology in vascular health and disease.

中文翻译：

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机械传导和炎症在血管稳态中的互补作用

动脉暴露于无休止的脉动性血液动力学负荷，但通过机械稳态，它们倾向于在健康成熟的长期内保持接近最佳的结构、特性和功能。然而，许多侮辱会损害这种稳态倾向，从而导致适应不良或疾病。慢性炎症可以算作动脉遭受的有害损伤，但炎症也可以发挥重要的稳态作用。在本文中，我们提出了一个新的理论模型，该模型对血管几何形状和组成以及特性和功能进行互补的机械生物学和免疫生物学控制。我们在常见的诱发性高血压小鼠模型中使用主动脉重塑数据来激发和说明该模型。预测与可用数据很好地匹配，注意到需要增加数据以进一步细化参数。然而，总体方法和结论是通用的，有助于统一两个以前完全不同的文献，从而更深入地了解机械生物学和免疫生物学在血管健康和疾病中的独立和重叠作用。