ArticleInternational journal of ophthalmology2026
Paeonol suppresses epithelial-mesenchymal transition-driven posterior capsular opacification through activation of AMPK signaling.
Article in International journal of ophthalmology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
aimTo determine whether paeonol (Pae), a naturally occurring phenolic compound, can serve as an effective pharmacological inhibitor of posterior capsular opacification (PCO).
methodsA rat model of cataract surgery-induced PCO was established, and Pae was administered
resultsPae significantly reduced capsular opacification and fibrotic remodeling in the rat PCO model compared with controls. In LECs, Pae markedly suppressed TGF-β2-induced EMT, evidenced by decreased expression of mesenchymal markers, such as Vimentin, Fibronectin, Collagen 1A1, α-SMA and preserved epithelial junctional protein ZO-1. Mechanistically, Pae was predicted to directly interact with the catalytic pocket of AMPK, which was experimentally confirmed by enhanced AMPK phosphorylation and nuclear translocation (
conclusionPae exerts a potent inhibitory effect on PCO formation by blocking EMT of LECs through direct activation of AMPK and subsequent disruption of TGF-β/Smad signaling.
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