Collagen is a vital component of the extracellular matrix of both the
heart and blood vessel walls. It acts as a scaffold to maintain in myo
cardial shape and permit an even distribution of force and plays a cru
cial role in the mechanical properties of the blood vessels. Under nor
mal circumstances, collagen is continually being synthesized and degra
ded through life. Increased mechanical stress, which causes myocardial
hypertrophy adn vessel was thickening, stimulates collagen turnover.
If collagen is deposited in excess (fibrosis), tissue function can be
compromised. An understanding of mechanisms of 'mechanosignal transduc
tion' involved in this process will enable therapeutic approaches to b
e devised that will prevent inappropriate collagen deposition and ther
eby help to preserve function.