Why the study?
While beta-catenin promotes cardiac fibrosis, the precise role of its homolog gamma-catenin in the fibrotic process remains largely unclear.
Does γ-catenin overexpression prevent cardiac fibrosis in preclinical models?
Does γ-catenin overexpression prevent cardiac fibrosis in preclinical models?
γ-catenin protects against cardiac fibrosis by inhibiting GSK-3β phosphorylation, offering a novel potential therapeutic target.
No immediate clinical implications for fibrosis; challenges β-catenin homology assumptions and leaves open distinct γ-catenin targeting.
Cardiac fibrosis is a common pathological change of many cardiovascular diseases. β-catenin has been shown to promote fibrosis. However, the precise role of its homolog γ-catenin in the process of fibrosis remains largely unclear. In this study, we found that the expression of γ-catenin was significantly decreased in angiotensin Ⅱ (Ang Ⅱ)-induced cardiac fibrosis model, contrary to most reports of β-catenin. Overexpression of γ-catenin in cardiac fibroblasts (CFs) significantly inhibited the expression of α-smooth muscle actin (α-SMA), whereas knocking down the expression of γ-catenin with siRNA promoted the occurrence of cardiac fibrosis. Mechanistically, γ-catenin could bind to GSK-3β to inhibit the phosphorylation of GSK-3β, therefore preventing cardiac fibrosis. Our study shows that γ-catenin is an important protective factor in cardiac fibrosis, which provides a new potential target for the treatment of cardiac fibrosis.
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Tang et al. (2019) studied this question.
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