| Summary: | Accumulating evidence indicates that two major proteins are responsible for the structural coherence of bounding cardiomyocytes. These biomolecules are known as myocardial fibrillar collagen type I (COL1) and type III (COL3). In addition, fibronectin, laminin, fibrillin, elastin, glycoproteins, and proteoglycans take part in the formation of cardiac extracellular matrix (ECM). In physiological conditions, collagen synthesis and degradation in human cardiac ECM are well-regulated processes, but they can be impaired in certain cardiovascular diseases, such as heart failure (HF). Myocardial remodeling is part of the central mechanism of HF and involves cardiomyocyte injury and cardiac fibrosis due to increased fibrillar collagen accumulation. COL1 and COL3 are predominantly involved in this process. Specific products identified as collagen-derived peptides are released in the circulation as a result of abnormal COL1 and COL3 turnover and myocardial remodeling in HF and can be detected in patients’ sera. The role of these products in the pathogenesis of cardiac fibrosis and the possible clinical implications are the focus of numerous investigations. This paper reviews recent studies on COL1- and COL3-derived peptides in patients with HF. Their potential application as indicators of myocardial fibrosis and prognostic markers of HF is also highlighted.
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