Endomyocardial expression of SDF-1 predicts mortality in patients with suspected myocarditis

Abstract

Endomyocardial expression of SDF-1 is enhanced in inflammatory cardiomyopathy, positively correlates with myocardial fibrosis and identifies high-risk patients with suspected myocarditis.

SDF‐1α (Stromal Cell‐Derived Factor 1α) Induces Cardiac Fibroblasts, Renal Microvascular Smooth Muscle Cells, and Glomerular Mesangial Cells to Proliferate, Cause Hypertrophy, and Produce Collagen

“…Importantly, in patients, circulating SDF-1a is associated with heart failure 29 and all-cause mortality, 30 and in patients with myocarditis, myocardial levels of SDF-1a are associated with cardiac fibrosis and are the strongest predictor of mortality. 31 The growing body of evidence that the SDF-1a/CXCR4 receptor axis contributes to organ fibrosis underscores the significance of the findings reported in this article.…”

DPP4 Inhibition, NPY1-36, PYY1-36, SDF-1α, and a Hypertensive Genetic Background Conspire to Augment Cell Proliferation and Collagen Production: Effects That Are Abolished by Low Concentrations of 2-Methoxyestradiol

“…The relevance of our finding is highlighted by the facts that in heart patients SDF-1a levels are increased and are associated with heart failure, cardiac fibrosis, and all-cause mortality (Chu et al, 2010;Subramanian et al, 2014;Zuern et al, 2015). Studies in mice reveal that antagonism of the CXCR4 receptor (receptor for SDF-1a) promotes myocardial tissue repair and reduces myocardial scarring after myocardial infarction .…”

“…This is a key question because in patients with cardiovascular diseases, some will have hypertension with coelevation of NPY 1-36 , PYY 1-36 , and SDF-1a. For example, in heart patients, SDF-1a levels are increased and are associated with heart failure, cardiac fibrosis, and allcause mortality (Chu et al, 2010;Subramanian et al, 2014;Zuern et al, 2015). Simultaneously, the release of NPY 1-36 from sympathetic nerves is augmented in heart failure (Hulting et al, 1990;Kaye et al, 1994).…”

Changes of myocardial gene expression and protein composition in patients with dilated cardiomyopathy after immunoadsorption with subsequent immunoglobulin substitution

“…The extent of myocardial fibrosis in EMB was determined from samples immediately fixed under sterile conditions in 4 % buffered formaldehyde by routine light microscopy examination using Masson's trichrome staining. The extent of myocardial fibrosis in EMB was defined as an index as described previously [58]. The percentage area of fibrosis in the section was evaluated by dividing the sum of fibrotic areas of the section by that of the total tissue area.…”