Email updates

Keep up to date with the latest news and content from BMC Systems Biology and BioMed Central.

This article is part of the supplement: The International Conference on Intelligent Biology and Medicine (ICIBM): Systems Biology

Open Access Research

Mathematical modeling of left ventricular dimensional changes in mice during aging

Tianyi Yang12, Ying Ann Chiao134, Yunji Wang2, Andrew Voorhees15, Hai-Chao Han15, Merry L Lindsey13 and Yu-Fang Jin12*

Author Affiliations

1 San Antonio Cardiovascular Proteomics Center, The University of Texas Health Science Center at San Antonio, USA

2 Department of Electrical and Computer Engineering, The University of Texas at San Antonio, USA

3 Barshop Institute of Longevity and Aging Studies; Division of Geriatrics, Gerontology and Palliative Medicine, Department of Medicine, The University of Texas Health Science Center at San Antonio, USA

4 Department of Biochemistry, The University of Texas Health Science Center at San Antonio, USA

5 Department of Mechanical Engineering, The University of Texas at San Antonio, USA

For all author emails, please log on.

BMC Systems Biology 2012, 6(Suppl 3):S10  doi:10.1186/1752-0509-6-S3-S10

Published: 17 December 2012

Abstract

Cardiac aging is characterized by diastolic dysfunction of the left ventricle (LV), which is due in part to increased LV wall stiffness. In the diastolic phase, myocytes are relaxed and extracellular matrix (ECM) is a critical determinant to the changes of LV wall stiffness. To evaluate the effects of ECM composition on cardiac aging, we developed a mathematical model to predict LV dimension and wall stiffness changes in aging mice by integrating mechanical laws and our experimental results. We measured LV dimension, wall thickness, LV mass, and collagen content for wild type (WT) C57/BL6J mice of ages ranging from 7.3 months to those of 34.0 months. The model was established using the thick wall theory and stretch-induced tissue growth to an isotropic and homogeneous elastic composite with mixed constituents. The initial conditions of the simulation were set based on the data from the young mice. Matlab simulations of this mathematical model demonstrated that the model captured the major features of LV remodeling with age and closely approximated experimental results. Specifically, the temporal progression of the LV interior and exterior dimensions demonstrated the same trend and order-of-magnitude change as our experimental results. In conclusion, we present here a validated mathematical model of cardiac aging that applies the thick-wall theory and stretch-induced tissue growth to LV remodeling with age.