Cell Biochemistry and Biophysics

, Volume 50, Issue 2, pp 53–78 | Cite as

Vascular Adaptation and Mechanical Homeostasis at Tissue, Cellular, and Sub-cellular Levels

  • J. D. HumphreyEmail author
Review Paper


Blood vessels exhibit a remarkable ability to adapt throughout life that depends upon genetic programming and well-orchestrated biochemical processes. Findings over the past four decades demonstrate, however, that the mechanical environment experienced by these vessels similarly plays a critical role in governing their adaptive responses. This article briefly reviews, as illustrative examples, six cases of tissue level growth and remodeling, and then reviews general observations at cell-matrix, cellular, and sub-cellular levels, which collectively point to the existence of a “mechanical homeostasis” across multiple length and time scales that is mediated primarily by endothelial cells, vascular smooth muscle cells, and fibroblasts. In particular, responses to altered blood flow, blood pressure, and axial extension, disease processes such as cerebral aneurysms and vasospasm, and diverse experimental manipulations and clinical treatments suggest that arteries seek to maintain constant a preferred (homeostatic) mechanical state. Experiments on isolated microvessels, cell-seeded collagen gels, and adherent cells isolated in culture suggest that vascular cells and sub-cellular structures such as stress fibers and focal adhesions likewise seek to maintain constant a preferred mechanical state. Although much is known about mechanical homeostasis in the vasculature, there remains a pressing need for more quantitative data that will enable the formulation of an integrative mathematical theory that describes and eventually predicts vascular adaptations in response to diverse stimuli. Such a theory promises to deepen our understanding of vascular biology as well as to enable the design of improved clinical interventions and implantable medical devices.


Mechanotransduction Mechanobiology Remodeling Stress Strain Arteries Endothelial cells Smooth muscle cells Fibroblasts 



This work was supported, in part, by grants from the NIH (HL-64372, HL-76319, HL-80415). I would also like to acknowledge general contributions to this work by former and current students, S. Baek, R. Gleason, S. Na, and A. Valentin, and excellent artwork by Nathalia de la Hoz.


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© Humana Press Inc. 2007

Authors and Affiliations

  1. 1.Department of Biomedical Engineering, 337 Zachry Engineering CenterTexas A&M UniversityCollege StationUSA

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