Galectin-3 as a potential biomarker for diabetic cardiomyopathy

Diabetic cardiomyopathy (DCM) is a common complication of type 2 diabetes mellitus (T2DM) characterized by myocardial fibrosis and diastolic dysfunction, with a high mortality as the disease progresses. Biomarkers can help detect DCM in the early stages for timely intervention. Galectin-3 (gal-3) is a β-galactoside-binding lectin that plays a key role in fibrosis and inflammation. We hypothesized that elevated levels of galectin-3 are associated with cardiac dysfunction and remodeling, promoting the development of DCM. We induced T2DM in male and female Sprague Dawley rats using a high-fat diet and a one-time intraperitoneal injection of streptozocin (30 milligrams per kilogram (mg/kg)). Cardiac mRNA expression of galectin-3 and atrial natriuretic peptide (ANP) (two cardiac hypertrophy markers) was determined by real-time polymerase chain reaction. Left ventricular function was measured by placing a Millar transducer into the left ventricle. Hematoxylin-eosin and Masson-trichrome staining of the left ventricle were used to assess myocardial structural changes and fibrosis. There were elevated levels of galectin-3 (2.24 ± 0.82) and ANP (10.10 ± 2.40) mRNAs in T2DM, compared to sham (1.49 ± 0.57 and 1.11 ± 0.22, respectively). Left ventricular end-diastolic pressure was higher in T2DM than that in sham (25.1 ± 2.8 vs. 3.3 ± 0.3 mm Hg). T2DM also induces cardiac hypertrophy and fibrosis. These findings suggest that an elevated level of galectin-3 is associated with myocardial hypertrophy and diastolic dysfunction and is a potential biomarker for DCM. Future studies would measure the protein expression of galectin-3 in T2DM throughout disease progression and utilize echocardiography to assess cardiac function. R01HL168500 to YLL This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.