Mechanical stimulation of micro-vascular endothelial cells contributes to lung remodelling in chronic heart failure

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Shortness of breath in longstanding heart failure occurs partly because the lungs become scarred and stiff, with the result that they are more difficult to expand and work less efficiently. When heart function is impaired, most commonly after a heart attack, the pressure in blood vessels draining into the heart increases and they become distended. I propose that stretching of these blood vessels contributes to lung scarring in longstanding heart failure. Our research team has developed a model that allows us to examine the consequences of stretching the cells that line small blood vessels. Using this model, I shall investigate the effect of stretch on the release of substances from cells that promote scar formation. We hope to identify the cause of lung scarring in heart failure with a view to discovering new targets for improving the lives of patients suffering from this very common and debilitating condition.