Endoglin has now been shown to be an important target of therapy to reduce disease symptoms associated with heart failure, particularly cardiac fibrosis. Soluble Endoglin is identified as an anatogonist to TGFβ1 activity, while membrane-bound Endoglin is identified as a necessary component to promote TGFβ1 activity in heart failure. The present invention therefore features methods and kits for treatment of subject having heart failure or a related disorder by administering a composition that decreases TGFβ1 signaling through either direct inhibition of membrane-bound Endoglin or promoting expression of soluble Endoglin.