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Elastin in the Arterial ECM: Interactions With Collagen and the Mechanical Properties After Elastin Degradation

[+] Author Affiliations
Ming-Jay Chow, Katherine Yanhang Zhang

Boston University, Boston, MA

Raphaël Turcotte

Boston University, Boston, MAMassachusetts General Hospital, Harvard Medical School, Boston, MA

Paper No. SBC2013-14257, pp. V01BT65A002; 2 pages
doi:10.1115/SBC2013-14257
From:
  • ASME 2013 Summer Bioengineering Conference
  • Volume 1B: Extremity; Fluid Mechanics; Gait; Growth, Remodeling, and Repair; Heart Valves; Injury Biomechanics; Mechanotransduction and Sub-Cellular Biophysics; MultiScale Biotransport; Muscle, Tendon and Ligament; Musculoskeletal Devices; Multiscale Mechanics; Thermal Medicine; Ocular Biomechanics; Pediatric Hemodynamics; Pericellular Phenomena; Tissue Mechanics; Biotransport Design and Devices; Spine; Stent Device Hemodynamics; Vascular Solid Mechanics; Student Paper and Design Competitions
  • Sunriver, Oregon, USA, June 26–29, 2013
  • Conference Sponsors: Bioengineering Division
  • ISBN: 978-0-7918-5561-4
  • Copyright © 2013 by ASME

abstract

Elastin and collagen are the main structural components in the extracellular matrix (ECM) that contribute to the anisotropic and hyperelastic passive mechanical behavior of elastic arteries. It is commonly accepted that the elastin fibers support most of the load at the onset of stretching while collagen fiber recruitment and the transition to collagen bearing the load occurs at higher pressures [1]. Various diseases lead to changes in the ECM, for example in aortic aneurysm there is reduced elastin, excess aged collagen, and fragmentation of the elastic lamellae [2]. Likewise hypertension has been shown to increase arterial collagen and wall thickness with increased stiffness [3]. Improving our knowledge of how the ECM structure affects the mechanical behavior of arteries can provide insights to disease progression and better treatment methods.

Copyright © 2013 by ASME

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