ArticleRedox report : communications in free radical research2025
Verbascoside targets endothelial HIF-1α/ Lysyl oxidase signaling to attenuate glomerular injury in diabetic nephropathy.
Article in Redox report : communications in free radical research, 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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Authors and funding
10 authors.
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Abstract
backgroundDiabetic nephropathy (DN) drives progressive renal fibrosis and functional decline, ultimately leading to end-stage renal disease. Pathological crosstalk between glomerular endothelial cells and mesangial cells is increasingly recognized as central to DN progression. However, whether endothelial-derived signaling specifically drives mesangial injury under diabetic conditions remains undefined.
methodsWe applied multi-omics profiling to identify pathogenic drivers. Target validation included qPCR and immunofluorescence co-localization in renal tissues.
resultsLOX/LOXL2 was robustly upregulated in diabetic endothelia. Inhibiting endothelial-derived LOX/LOXL2 or HIF-1α in GECs attenuated HG-induced mesangial dysfunction by reducing proliferation/viability, oxidative stress, and fibrosis. Mechanistically, HIF-1α drove LOX/LOXL2 expression. VB was identified as a novel dual LOX/LOXL2 inhibitor. VB-CM mitigated mesangial injury
conclusionEndothelial HIF-1α/LOX signaling drives mesangial oxidative stress and fibrosis in DN. Verbascoside, a dual LOX/LOXL2 inhibitor, represents a promising therapeutic agent targeting this pathogenic axis.
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