Abstract
Collagen is a vital component of the extracellular matrix of both the heart and blood vessel walls. It acts as a scaffold to maintain myocardial shape and permit an even distribution of force, and plays a crucial role in the mechanical properties of the blood vessels. Under normal circumstances, collagen is continually being synthesized and degraded throughout life. Increased mechanical stress, which causes myocardial hypertrophy and vessel wall thickening, stimulates collagen turnover. If collagen is deposited in excess (fibrosis), tissue function can be compromised. An understanding of the mechanisms of 'mechanosignal transduction' involved in this process will enable therapeutic approaches to be devised that will prevent inappropriate collagen deposition and thereby help to preserve function.
Published Version
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