Biomechanical basis of vascular tissue engineering.
Blood vessels develop under the influence of mechanical stresses and strains and remodel in response to alterations in these factors. It has long been hypothesized that mechanical stresses and strains contribute to the development of vascular diseases such as atherosclerosis and hypertrophy. A large number of studies have been conducted to verify this hypothesis and have demonstrated that increased tensile stress and strain due to hypertension may induce and/or facilitate vascular hypertrophy, and oscillatory low fluid shear stress and/or altered shear gradients due to eddy blood flow may initiate and/or promote focal atherosclerosis and intimal hyperplasia. A variety of cellular components, including growth-related factors, cell membrane proteins and lipids, intracellular signaling molecules and transcriptional factors, and immediate early genes and mitogenic genes, have been shown to mediate these mechanical stress-related pathological processes. These discoveries suggest that a modulation of tensile and fluid shear stresses and strains, if possible, may prevent mechanical stress-induced pathological changes in blood vessels and thus constitute a foundation for the development of vascular engineering approaches. Recent studies have demonstrated by using an experimental vein graft model that biomechanical engineering approaches can be used to reduce tensile stress and strain due to exposure to arterial blood pressure and to prevent eddy blood flow in vein grafts. Such engineering modulations significantly reduced the rate of focal intimal hyperplasia and medial and adventitial hypertrophy in vein grafts. These preliminary studies have provided convincing evidence for further development of vascular biomechanical engineering approaches. In this article, the background, principles, clinical potentials, as well as the limitations of vascular biomechanical engineering are discussed.
Liu
S Q
SQ
Biomedical Engineering Department, Northwestern University, Evanston, IL 60208-3107, USA.
D001161:Arteriosclerosis / Q000150:complications / Q000175:diagnosis / Q000503:physiopathology* / Q000628:therapy; D001696:Biomechanical Phenomena; D004730:Endothelium, Vascular / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D006965:Hyperplasia; D006973:Hypertension / Q000150:complications / Q000503:physiopathology; D008955:Models, Cardiovascular; D015398:Signal Transduction; D013314:Stress, Mechanical; D013718:Tensile Strength