ArticleJournal of translational medicine2026
Involvement of Fibulin-5 in endothelial to mesenchymal transition leading to cardiac fibrosis during metabolic syndrome.
Article in Journal of translational medicine, 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
backgroundCardiac fibrosis is a hallmark of metabolic syndrome, a condition linked to Western lifestyles and high cardiovascular risk. We previously demonstrated that dietary sodium restriction prevents cardiac fibrosis and remodeling in a rat model of metabolic syndrome through reduced macrophage infiltration. Here, we investigate genes involved in endothelial-to-mesenchymal transition (EndoMT), a key process in cardiac fibrosis.
methodsMetabolic syndrome was induced in rats by high-fructose feeding combined with angiotensin II infusion. EndoMT was assessed in left ventricles and in vitro using TGF-β2-treated human aortic (HAEC) and umbilical vein endothelial cells (HUVEC) via immunofluorescence, western blotting, and RT-qPCR. Lentiviral shRNA was used to knock down target genes.
resultsSodium restriction reduced vascular EndoMT in rat left ventricles and downregulated several candidate genes. In vitro, Fibulin-5, a matricellular protein, was markedly upregulated during EndoMT. Silencing Fibulin-5 prevented TGF-β2-induced EndoMT in HAEC and HUVEC, indicating its essential role. Mechanistically, Fibulin-5 modulated SMAD2/3, ERK1/2, and p38 MAPK pathways. In vivo, Fibulin-5 expression was significantly reduced in aortic intima and plasma of sodium-restricted rats.
conclusionFibulin-5 emerges as a potential mediator of vascular EndoMT and cardiac fibrosis through TGF-β signaling modulation. Dietary sodium restriction mitigates this process, highlighting Fibulin-5 as a potentially important contributor in metabolic syndrome-related cardiac remodeling.
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