ArticleFuture science OA2025
Hesperidin alleviates pulmonary fibrosis by regulating EI24-mediated autophagy.
Article in Future science OA, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
- Recent insights into the biological functions of hesperidin.EXCLI journal · 2025Article
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3 authors.
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Abstract
backgroundEtoposide-induced protein 2.4 (EI24), an essential component of autophagy, is lowly expressed in pulmonary fibrosis. Hesperidin (Hes), a flavonoid, can regulate autophagy in various diseases. However, whether Hes can inhibit pulmonary fibrosis by mechanically regulating EI24-mediated autophagy has not been uncovered.
methodsRLE-6TN cells were treated with transforming growth factor β1 (TGF-β1) and rats were injected with bleomycin (BLM) to construct the pulmonary fibrosis model. The effect of Hes on pulmonary fibrosis was evaluated by cell counting kit-8, immunofluorescence, hematoxylin and eosin, masson trichome staining and western blotting.
resultsHes reduced cell viability of TGF-β1-induced RLE-6TN cells. Administration of Hes restored the decrease in autophagy marker levels in TGF-β1-induced RLE-6TN cells. Hes inhibited the transcriptional and translational levels of α-SMA, collagen I and fibronectin that were increased by TGF-β1 in RLE-6TN cells. Mechanically, Hes restored EI24 expression, and EI24 knockdown reversed the effect of Hes on the expressions of autophagy and fibrosis-related proteins. Additionally, Hes enhanced autophagy and fibrosis markers, which were worsened by EI24 knockdown in BLM-induced rats.
conclusionHes activated autophagy by upregulating EI24, which improved pulmonary fibrosis both
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