Key result
Galectin-3 knockdown decreases cardiac dysfunction in diabetic mice by reducing myocardial inflammation and fibrosis.
Why the study?
Galectin-3 regulates cardiac inflammation and fibrosis, but its role in diabetic cardiomyopathy remains unclear.
Does Gal-3 inhibition ameliorate cardiac injury, fibrosis, and dysfunction in a mouse model of diabetic cardiomyopathy?
Does Gal-3 inhibition ameliorate cardiac injury, fibrosis, and dysfunction in a mouse model of diabetic cardiomyopathy?
Galectin-3 inhibition attenuates diabetic cardiomyopathy in mice by reducing inflammation, fibrosis, and apoptosis via suppression of the NF-κB p65 pathway.
Gal-3 inhibition attenuates diabetic cardiomyopathy in mice; leaves open translation to human therapy.
Objective: Diabetic cardiomyopathy (DCM), characterized by cardiomyopathy with the absence of coronary artery disease, hypertension, and valvular heart disease in patients with diabetes, significantly increases the risk of heart failure. Galectin-3 (Gal-3) has been shown to regulate cardiac inflammation and fibrosis, but its role in DCM remains unclear. This study aimed to determine whether Gal-3 inhibition attenuates DCM and NF-κB p65 activation. Methods: . The terminal deoxyribonucleotide transferasemediated dUTP nick end-labeling (TUNEL) and immunofluorescence assays were conducted to examine myocardial apoptosis and oxidative stress. Inflammatory cytokines induced by high glucose (HG) were also found in RAW264.7 macrophages. The underlying molecular mechanisms were determined using immunofluorescence and Western blotting analyses. Results: The Gal-3 knockdown was observed to ameliorate myocardial apoptosis, oxidative stress, inflammatory cytokines release, macrophage infiltration, and fibrosis, thus, decreasing cardiac dysfunction in DCM mice. In addition, the silence of Gal-3 could suppress macrophage infiltration and inflammatory cytokine release induced by HG. Finally, a Gal-3/NF-κB p65 regulatory network was clarified in the pathogenesis of DCM. Conclusion: by the mechanism of reduction of NF-κB p65 activation.
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Zhu et al. (2022) studied Diabetic cardiomyopathy. AAV9-Gal-3 (Adeno-associated virus 9 incorporating Gal-3-short hairpin RNA) vs. AAV9-NC (scrambled-shRNA) or vehicle was evaluated on Cardiac structure and function, myocardial injury markers, fibrosis, and inflammation (p=<0.05). Galectin-3 knockdown ameliorated myocardial apoptosis, oxidative stress, inflammatory cytokine release, macrophage infiltration, and fibrosis, decreasing cardiac dysfunction in diabetic mice.
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