Abstract

In common with most dynamic tissues, the mechanical properties of arteries are determined by the relative composition and architecture of key structural extracellular matrix (ECM) proteins including fibrillar collagens and elastic fibre components. Although it is apparent that age-related loss of ECM homeostasis leads to arteriosclerosis (vascular stiffening), which in turn is associated with the development of both fatal strokes and heart failure, the principal molecular targets and causative mechanisms remain poorly defined. This review discusses: (i) the application of in situ micro-mechanical methodologies to localise the key molecular targets of age-related stiffening within arteries and other dynamic elastic tissues and (ii) the potential role played by the preferential oxidation of TGF-β binding elastic fibre-associated components in driving this aberrant tissue remodelling.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call