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Figure 2. DEGs in ECs during DCM pathogenesis. Prolonged hyperglycemia in diabetes results in altered gene expression, preceding ED and subsequent microvascular injury. In general, these genes can be classified into six functional categories based on vascular pathology, including inflammation, oxidative stress response, complement activation, fibrosis, angiogenesis, and lipid metabolism^[14,22,23]. Overlapping gene pathway assignments are supported by GO/KEGG analyses [Supplementary Table 1], with additional functional validation from experimental literature. DEG: Differentially expressed gene; DCM: diabetic cardiomyopathy; EC: endothelial cell; ED: endothelial dysfunction; GO: gene ontology; KEGG: kyoto encyclopedia of genes and genomes; MAPK: mitogen-activated protein kinase; JAK: Janus kinase. STAT: signal transducers and activators of transcription; NLRP3: nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3; PPAR-γ: peroxisome proliferator-activated receptor γ; BCL2: B-cell lymphoma 2; HIF-1: hypoxia-inducible factor 1; VEGF: vascular endothelial growth factor; IP3R: inositol 1,4,5-trisphosphate receptor; TGF: transforming growth factor; PDGFR: Platelet-derived growth factor receptor; SMAD: Sma- and Mothers against decapentaplegic-related proteins [Created in BioRender. Justin R (2025)].