A Biomarker of Inflammation, Fibrosis, Cardiovascular Diseases, Metabolic Syndrome and Tumor

Using galectin-3 to reduce heart failure rehospitalization

Increasing attention is being paid towards reducing short-term heart failure readmissions in recent years. Biomarkers such as galectin-3 are likely to play pivotal roles in future heart failure management strategies as they can provide objective information on various pathophysiologic processes involved in heart failure. Galectin-3 is a biomarker of inflammation and fibrosis, which is strongly associated with adverse remodeling of the myocardium and subsequent left ventricular dysfunction. Clinically, elevated galectin-3 levels are associated with increased risk for short- and long-term risk for mortality and heart failure readmission. Galectin-3 can provide incremental predictive value for adverse events over natriuretic peptides. Although significant work is still required to further define the role of galectin-3, it has the potential to become an important part of future heart failure management algorithms by helping to provide an individualized risk profile, which can be used to optimize resource allocation and improve treatment outcomes.

Xue, Y, et al. Future Cardiol. 2014 Mar;10(2):221-7. doi: 10.2217/fca.14.9.

Galectin-3 plays a role in atherosclerotic diseases, and the effect of adiponectin that protects from atherosclerotic diseases on monocytic galectin-3 was analysed. Adiponectin reduced galectin-3 mRNA, its cellular and soluble form, and this effect was impaired in T2D cells. Cellular galectin-3 was higher in monocytes of overweight than normal-weight donors and was highest in T2D cells. Cellular galectin-3 positively correlated with the BMI of the donors and negatively with soluble monocyte galectin-3. Circulating levels of total adiponectin did not correlate with cellular or soluble galectin-3 indicating that additional factors contribute to higher cellular monocytic galectin-3 in obesity and T2D.