Therapeutic inhibition of galectin‑3 improves cardiomyocyte apoptosis and survival during heart failure.

Galectin-3 is an important mediator of cardiac fibrosis and heart failure. Cell viability of cardiomyocytes was measured using a CCK‑8 assay; flow cytometry was employed for the detection of the cell cycle and cardiomyocytes apoptosis. Reverse transcription‑quantitative polymerase chain reaction and western blotting was performed to examine the expression of associated genes and proteins. The present study demonstrated that overexpression of galectin‑3 significantly decreased the viability of cardiomyocytes in a time‑dependent manner, with simultaneous arrest of the cell cycle and induction of apoptosis. The expression levels of proliferating cell nuclear antigen (PCNA) and B‑cell lymphoma 2 (Bcl‑2) were decreased and Bcl‑2‑associated X protein (Bax) was increased in cardiomyocytes with galectin‑3 overexpression. However, inhibition of galectin‑3 by intravenous tail vein injection of a galectin‑3‑targeting short hairpin RNA‑expressing vector during hypertension‑induced heart failure in Dahl hypertensive rats increased rat survival and body weight. Inhibition of galectin‑3 also increased the expression of PCNA and Bcl‑2 and reduced the expression of Bax in the cardiac tissue of hypertensive rats. These results demonstrate the therapeutic potential of targetinggalectin‑3 for the treatment of cardiac disease.