ArticleAmerican journal of translational research2026
Diosgenin mitigates laser-induced choroidal neovascularization by suppressing the endothelial-to-mesenchymal transition via the TGF-β/Smad and MAPKs signaling pathways.
Article in American journal of translational research, 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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12 authors.
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Abstract
objectivesTo explore whether diosgenin (Dio), a natural steroidal saponin, alleviates laser-induced choroidal neovascularization (CNV) and its underlying mechanism related to endothelial to mesenchymal transition (EndMT) and signaling pathways.
methodsA mouse model of laser-induced CNV was established; mice were treated with Dio (50 μM, 100 μM) or ranibizumab. In vitro, human umbilical vein endothelial cells (HUVECs) were stimulated with oxidized low-density lipoprotein (Ox-LDL) and pretreated with Dio. CNV leakage, lesion size, EndMT markers, and TGF-β/Smad and MAPKs pathway activities were detected by fundus angiography, Western blot, Transwell, and tube formation assays.
resultsDio reduced CNV leakage and lesion area in mice, inhibited HUVEC migration and tube formation. It downregulated mesenchymal markers (α-SMA, vimentin), upregulated endothelial markers (VE-cadherin, ZO-1), and suppressed phosphorylation of Smad2/3, p38, ERK1/2, and JNK.
conclusionsDio mitigates laser-induced CNV by inhibiting EndMT via the TGF-β/Smad and MAPKs signaling pathways, serving as a potential candidate for neovascular age-related macular degeneration.
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