Heart failure is one of the most costly health problems worldwide. A hallmark of heart failure is cardiac fibrosis, an abnormal and persistent accumulation of scar tissue (mainly the extracellular matrix protein, collagen) that significantly impairs heart function.

Although heart failure can be caused by many disease processes, there is always a degree of fibrosis when heart failure occurs. It has recently been recognised that the mechanism by which fibrosis occurs is different in different disease states. This likely explains the reason that heart failure treatments are effective in some causes of heart failure, but not in others. A deeper understanding of the different cellular and molecular processes causing this build up of scar tissue is needed if we are to rationally design new medical therapies for heart failure of all different causes. Identification of new molecules that contribute the cardiac fibrosis will ultimately lead to new drugs designed to prevent fibrosis. This has the potential to save millions of lives and billions of dollars.

One potential target is the secreted extracellular matrix protein, fibulin-3 (Fib3), which is expressed in human and mouse hearts, however its role in cardiac biology is incompletely understood. We have recently shown a significant increase of Fib3 levels the mouse heart both in ageing and after myocardial infarction (MI) i.e. a heart attack. In vitro, we have demonstrated that Fib3 is released by cardiac fibroblasts (cFb), the cells that make scar tissue, and that it leads to production of collagen and other scar-related proteins. Taken together, our preliminary data represent compelling evidence for Fib3 as a potential therapeutic target in the cardiac fibrosis associated with heart failure.

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