Fig. 3

Lumican accelerates adverse cardiac remodeling by inhibiting TGFβ/Smad signaling. (A, B) KEGG enrichment analysis of DEGs between patients with heart failure and healthy individuals (A) and between patients with gout and healthy individuals (B), (C) Serum levels of active TGF-β1 detected by ELISA in hyperuricemic mice after MI surgery (n = 6). (D) Western blot analysis of p-Smad2, total Smad2, p-Smad3, total Smad3, and Smad4 in the infarcted area of hyperuricemic mice after MI surgery. (E, F) Quantitative analysis of p-SMAD2 and p-SMAD3 expression (n = 6). (G) α-SMA mRNA expression in the infarcted area of hyperuricemic mice after MI surgery was assessed via qPCR. (H) Western blot analysis of α-SMA, collagen 1, and fibronectin in the infarct area of hyperuricemic mice after MI surgery. (I, J) Immunofluorescence staining and quantification of α-SMA, collagen 1, and fibronectin levels in the infarct areas of hyperuricemic mice after MI surgery. The data are expressed as the means ± standard errors. Statistical analysis was performed via Student’s t test. *p < 0.05. DEG, differentially expressed gene; KEGG, Kyoto Encyclopedia of Genes and Genomes; MI, myocardial infarction