Pressure overload in a murine model generated a unique profile of cardiac tissue-specific and plasma-derived inflammatory mediators compared to silica-induced lung fibrosis.
Chronic pressure overload in mice generates a unique, cardiac-specific profile of inflammatory mediators distinct from other fibrotic processes like lung fibrosis.
Myocardial fibrosis and the resultant increases in myocardial stiffness represent pivotal consequences of chronic pressure overload (PO). In this study, cytokine profiles produced in a murine model of cardiac fibrosis induced by PO were compared with those produced in response to silica-induced lung fibrosis. A unique profile of cardiac tissue-specific and plasma-derived factors generated in response to PO are reported.
O’Brien et al. (Fri,) conducted a other in Cardiac fibrosis induced by pressure overload. Pressure overload vs. Silica-induced lung fibrosis was evaluated on Cytokine profiles. Pressure overload in a murine model generated a unique profile of cardiac tissue-specific and plasma-derived inflammatory mediators compared to silica-induced lung fibrosis.