We have investigated factors responsible for increased circulating Gal-3 in cardiomyopathy by addressing the following questions: First, whether changes in circulating Gal-3 levels is aetiology-dependent; Second, whether the inflammatory state of heart disease is associated with increased circulating Gal-3; Third, whether activation of β-ARs alters cardiac and circulating Gal-3 levels; Finally, whether there is Gal-3 release from the heart into the circulation. Here, CTBP1 is linked to cardiomyopathy.