Abstract
Aortic aneurysms are among the most critical cardiovascular diseases. The present study is focused on ascending thoracic aortic aneurysms (ATAAs). The main causes of ATAAs are cardiac malformations such as a bicuspid aortic valve or genetic mutations. Research studies dedicated to ATAA tend more and more to invoke multifactorial effects. In the current review, we show that all these effects converge toward a single paradigm relying upon the crucial biomechanical role played by smooth muscle cells (SMCs) in controlling the distribution of mechanical stresses across the aortic wall. The chapter is organized as follows. In Section 6.2, we introduce the basics of arterial wall biomechanics and how the stresses are distributed across its different layers and among the main structural constituents: collagen, elastin, and SMCs. In Section 6.3, we introduce the biomechanical active role of SMCs and its main regulators. We show how SMCs actively regulate the distribution of stresses across the aortic wall and among the main structural constituents. In Section 6.4, we review studies showing that SMCs tend to have a preferred homeostatic tension. We show that mechanosensing can be understood as a reaction to the homeostasis unbalance of SMC tension. Through the use of layer-specific multiscale modeling of the arterial wall, it is revealed that the quantification of SMC homeostatic tension is crucial to predict numerically the initiation and development of ATAA.
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