Knockdown of eIF3a ameliorates cardiac fibrosis by inhibiting the TGF-β1/Smad3 signaling pathway.

eIF3a expression was significantly up-regulated in TGF-β1-induced cardiac fibroblasts.

• Cardiac fibroblasts play a crucial role in the development of cardiac fibrosis.
• The study found that knocking down eIF3a reduced TGF-β1-induced cardiac fibroblast proliferation.
• Silencing eIF3a led to decreased levels of α-smooth muscle actin and SM22α, markers associated with myofibroblast differentiation.
• Inhibition of eIF3a also decreased the activation of Smad3, a protein involved in the fibrogenesis process.
• These findings indicate that targeting eIF3a may provide a new approach for managing cardiac fibrosis.

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