Circulating levels of procollagen type I carboxy‐terminal propeptide reflect myocardial fibrosis

Abstract

This article refers to 'The combination of carboxyterminal propeptide of procollagen type I blood levels and late gadolinium enhancement at cardiac magnetic resonance provides additional prognostic information in idiopathic dilated cardiomyopathy -A multilevel assessment of myocardial fibrosis in dilated cardiomyopathy' by A.G. Raafs et al., published in this issue on pages 933-944.Myocardial fibrosis is a consequence of a profound change in the architecture and composition of the cardiac extra-cellular matrix affecting the structure and function of the heart. Non-specific insults to the cardiovascular system (e.g. hypertension, diabetes, ageing, ischaemia, genetic alterations) may dysregulate various cell types and signalling pathways, ultimately resulting in myocardial fibrosis. 1,2 Once established, myocardial fibrosis is strongly associated with a poor prognosis, including in patients with idiopathic dilated cardiomyopathy (DCM). 3,4 Despite the sound pathophysiological background and prognostic impact of myocardial fibrosis, its assessment remains challenging in clinical practice. Circulating markers reflecting collagen synthesis are under investigation as potential means for evaluating myocardial fibrosis non-invasively. In this regard, procollagen type I carboxy-terminal propeptide (PICP) may directly reflect the synthesis of collagen type 1 because it is produced during the conversion of procollagen type I to collagen type I in a 1:1 ratio. 1 Furthermore, serum PICP levels have been correlated with total myocardial collagen volume fraction (CVF) (assessed in myocardial samples with collagen-specific staining) in patients with hypertension, heart failure and DCM. 4,5 Another potential marker of collagen synthesis is N-terminal propeptide of type III collagen (PIIINP). PIIINP is generated from the conversion of procollagen type III into collagen type III and has been correlated with the amount of collagen type III fibres in the myocardium of heart failure patients, but itThe opinions expressed in this article are not necessarily those of the Editors of the European Journal of Heart Failure or of the European Society of Cardiology.

The protective effect of zinc, selenium, and chromium on myocardial fibrosis in the offspring of rats with gestational diabetes mellitus

“…Col-I is a major contributor to myocardial stiffness and pathological myocardial fibrosis, and is composed of large-diameter fibers with a high cross-linking ability. 42 MMP-9, an important member of the matrix metalloproteinase family, plays a key role in stimulating collagen deposition in ECM and is closely related to the expression of pro-inflammatory genes and TGF-β signaling. 43 α-Smooth muscle actin (α-SMA) is involved in smooth muscle contraction, which is considered as the marker for the differentiation of cardiac fibroblasts into myofibroblasts.…”