Collagen: scaffold for repair or execution.

The shape, cellular arrangement and the tensile strength of organs are determined by their extracellular matrix (ECM) [l]. This consists of a variety of molecules, among which fibrillar collagens and proteoglycans quantitatively predominate. The cells of the connective tissue were formerly considered to be almost metabolically inactive, but are now recognised as being an active participant in the initiation and modulation of tissue growth and repair [l-4]. Under normal physiological conditions, the ECM undergoes constant maintenance, with a relatively low basic turnover. Damage to tissue, largely independent of aetiology and target organ, produces a uniform response resulting in repair, which dramatically increases the activity of connective tissue cells [5-71. Fundamentally, the process of repair serves to minimise the extent of initial damage and to preserve organ function. Increased collagen synthesis is an important part of this process. Despite the intention to save organ function, the outcome may be a twoedged sword: in an effort to save the organ, re-establishment of normal function is impaired by increased amounts of collagen. In cardiovascular diseases, the reduced contractility in the zone adjacent to a myocardial infarct [8,9], the stiffness of the myocardium in hypertrophied cardiomyopathies, and the reduced compliance of the arteries in hypertension, are all examples of impaired function brought about by the increased amounts of deposited collagen. Therefore, a better understanding of the role played by the connective tissue cells in cardiovascular diseases is essential if further diagnostic and therapeutic improvements are to be achieved. The promising reports on the collagen modulating effect of ACE inhibition and specific angiotensin II antagonists, clearly prompts this. Furthermore, thrombolytic therapy of acute myocardial infarction represent a clinical situation with pronounced influence on collagen metabolism. The first step towards management of unwanted fibrosis, without interfering with necessary repair is the development and validation of non-invasive methods for sequential measurement of extracellular activity, i.e. deposition and degradation of collagen. Serological markers of the collagen metabolism seems to constitute a good tool for forthcoming clinical research in the field. The current knowledge of serological markers of the collagen metabolism in cardiovascular diseases, is reviewed in the present article.