Multiscale Modeling in Vascular Disease and Tissue Engineering
The human body, and hence the vascular system, is by its very nature a dynamic multiscale hierarchial system. This multiscale nature encompasses different length scales, from molecular and cellular levels to the tissue and organ level, as well as differen
- PDF / 2,303,335 Bytes
- 18 Pages / 439.37 x 666.142 pts Page_size
- 59 Downloads / 268 Views
Abstract The human body, and hence the vascular system, is by its very nature a dynamic multiscale hierarchial system. This multiscale nature encompasses different length scales, from molecular and cellular levels to the tissue and organ level, as well as different physical phenomena, such as mechanical, biological and chemical processes. In arteries, vascular cells alter their growth, phenotype and extracellular matrix production in response to macro mechanical changes. These cell level events can in turn accumulate and emerge at the tissue level as pathological conditions such as atherosclerosis and intimal hyperplasia. These cardiovascular diseases evolve through adaptation of cells and tissues over days to months also demonstrating the multiscale nature of vascular diseases with respect to time. The challenge in vascular multiscale modelling is to create a framework which can incorporate the key mechanical, biological and chemical characteristics of this complex system at these various space and time scales to successfully capture the long-term behaviour of the system. Such a framework can then be used to gain additional insights with regards to pathological conditions within the vascular system and to improve the design of medical devices used to treat such pathologies. In the following chapter, a review will be presented of some relevant studies reported in literature which have used multiscale modelling approaches to elucidate the growth and remodelling mechanisms underlying vascular diseases, such as atherosclerosis, in-stent restenosis and intimal hyperplasia.
H. Zahedmanesh C. Lally (&) School of Mechanical and Manufacturing Engineering, Dublin City University, Glasnevin, Dublin 9, Ireland e-mail: [email protected]
Stud Mechanobiol Tissue Eng Biomater (2013) 14: 241–258 DOI: 10.1007/8415_2012_159 Ó Springer-Verlag Berlin Heidelberg 2012 Published Online: 10 November 2012
241
242
H. Zahedmanesh and C. Lally
1 Introduction Arterial growth, remodelling and vascular diseases are intrinsically multiscale and depend on the interactions occurring at the tissue level, cell level and the intracellular level. Consequently, multiscale computational modelling techniques can help to elucidate the mechanisms underlying the onset and progression of vascular diseases as well as vascular tissue regeneration. Mechanical perturbations at the tissue level translate to cell level mechanical signals via cell–matrix interactions. How these mechanical signals are further transduced through the cytoskeletal assembly, and other signalling pathways such as calcium channels to the cell nucleus, resulting in specific gene expressions which subsequently alter cellular behaviour, adds an additional level of complexity to these multiscale systems. Cells alter their growth, phenotype and their extracellular matrix in response to macro mechanical changes. These cell level events can then in turn accumulate and emerge at the tissue level as pathological conditions such as atherosclerosis and intimal hyperplasia. Multiscale modell
Data Loading...
