TY - JOUR
T1 - Extracellular matrix and the mechanics of large artery development
AU - Cheng, Jeffrey K.
AU - Wagenseil, Jessica E.
N1 - Funding Information:
Acknowledgments This work was supported, in part, by the National Institutes of Health (Grants R01 HL105314, R00 HL087563, and T32 HL007275). Robert Mecham is acknowledged for providing the Eln−/− and Eln+/− mice, invaluable advice, and editorial assistance. Attila Kovacs is acknowledged for obtaining the ultrasound images in Fig. 3. Russel Knusten and Marilyn Levy are acknowledged for assistance with the EM images in Fig. 1.
PY - 2012/11
Y1 - 2012/11
N2 - The large, elastic arteries, as their name suggests, provide elastic distention and recoil during the cardiac cycle in vertebrate animals. The arteries are distended from the pressure of ejecting blood during the active contraction of the left ventricle (LV) during systole and recoil to their original dimensions during relaxation of the LV during diastole. The cyclic distension occurs with minimal energy loss, due to the elastic properties of one of the major structural extracellular matrix(ECM)components, elastin.Themaximumdistension is limited to prevent damage to the artery by another major ECM component, collagen. The mix of ECM components in the wall largely determines the passive mechanical behavior of the arteries and the subsequent load on the heart during systole. While much research has focused on initial artery formation, there has been less attention on the continuing development of the artery to produce the mature composite wall complete with endothelial cells (ECs), smooth muscle cells (SMCs), and the necessary mix of ECM components for proper cardiovascular function. This review focuses on the physiology of large artery development, including SMC differentiation and ECM production. The effects of hemodynamic forces and ECM deposition on the evolving arterial structure and function are discussed. Human diseases and mouse models with genetic mutations in ECM proteins that affect large artery development are summarized. A review of constitutive models and growth and remodeling theories is presented, along with future directions to improve understanding of ECM and the mechanics of large artery development.
AB - The large, elastic arteries, as their name suggests, provide elastic distention and recoil during the cardiac cycle in vertebrate animals. The arteries are distended from the pressure of ejecting blood during the active contraction of the left ventricle (LV) during systole and recoil to their original dimensions during relaxation of the LV during diastole. The cyclic distension occurs with minimal energy loss, due to the elastic properties of one of the major structural extracellular matrix(ECM)components, elastin.Themaximumdistension is limited to prevent damage to the artery by another major ECM component, collagen. The mix of ECM components in the wall largely determines the passive mechanical behavior of the arteries and the subsequent load on the heart during systole. While much research has focused on initial artery formation, there has been less attention on the continuing development of the artery to produce the mature composite wall complete with endothelial cells (ECs), smooth muscle cells (SMCs), and the necessary mix of ECM components for proper cardiovascular function. This review focuses on the physiology of large artery development, including SMC differentiation and ECM production. The effects of hemodynamic forces and ECM deposition on the evolving arterial structure and function are discussed. Human diseases and mouse models with genetic mutations in ECM proteins that affect large artery development are summarized. A review of constitutive models and growth and remodeling theories is presented, along with future directions to improve understanding of ECM and the mechanics of large artery development.
KW - Aorta
KW - Biomechanics
KW - Collagen
KW - Elastin
UR - https://www.scopus.com/pages/publications/84870770165
U2 - 10.1007/s10237-012-0405-8
DO - 10.1007/s10237-012-0405-8
M3 - Article
C2 - 22584609
AN - SCOPUS:84870770165
SN - 1617-7959
VL - 11
SP - 1169
EP - 1186
JO - Biomechanics and Modeling in Mechanobiology
JF - Biomechanics and Modeling in Mechanobiology
IS - 8
ER -