The human heart has little capacity to repair or regenerate, and following the myocardial infarction injury the myocardium is replaced by non-contracting scar tissue.
Consequently, increased wall stress and workload on the remaining myocardium leads to chamber dilation, dysfunction, and ultimately heart failure.
Mechanobiology in Cardiovascular Tissue Engineering (Vincent Chan)
Cardiovascular diseases (CVD) such as hypertension affect a large portion of population in UAE (https://www.thenational.ae/uae/wealthy-uae-residents-significantly-more-at-risk-of-heart-disease-1.625049). Currently, the design of CVD therapy heavily relies on the use of cell culture and animal model which does not fully represent the physiology of vascular systems, e.g., blood vessel. Although 2D cell culture systems have been applied to probe the effect of mechanotransduction, e.g., contractile force generation, on cell migration, proliferation and metastatic potential, the development of tissue culture system for recapitulating the 3D histology of native tissues is necessary in order to raise the accuracy in drug target identification. In particular, it is known that the phenotypic shift of vascular smooth muscle cells in tunica media from contractile to synthetic state is correlated with the change of cell traction force pattern at the tissue level. Our work aims to optimize the cell culture conditions for triggering the expression of physiological functions in each tissue layer of blood vessel equivalents. In addition, the best possible design of engineered 3D geometry of the supporting biomaterial scaffold ranging from rectangular microwall to circular microchannel for promoting blood vessel’s plasticity found in vascular mechanotransduction will be elucidated. Our long-term goal is to capitalize on the mechanobiology for developing novel technological platform for CVD drug discovery. In parallel, such knowhow will enable the development of novel cardiovascular tissue equivalents for applications in regeneration medicine.