ArticlePharmacological reports : PR2026
Trimetazidine modulates angiogenesis, inflammation, and metabolism-related gene expression to promote diabetic foot ulcer healing: a transcriptomic analysis.
Article in Pharmacological reports : PR, 2026. 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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Who cites it
1 citing paper in PubMed.
- Multidimensional Regulatory Mechanisms and Targeted Therapeutic Strategies for Inhibited Keratinocyte Proliferation in Diabetic Wounds.Drug design, development and therapy · 2026Review
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Authors and funding
5 authors.
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Abstract
backgroundDiabetic foot ulcers (DFUs) are a chronic complication of diabetes associated with impaired healing and tissue ischemia.
aimThis study explores the transcriptional effects of trimetazidine (TMZ) in wound-relevant human cell models to generate hypotheses regarding its potential mechanisms of action.
methodsWe conducted a secondary analysis of LINCS Phase 5 transcriptomic data to evaluate TMZ-induced gene expression in four human cell lines relevant to DFU pathophysiology: HUVEC (endothelial), THP1 (monocytic), A375 (keratinocytic-like), and MCF7 (epithelial-like).
resultsTMZ induced 700-900 differentially expressed genes per cell line, with distinct yet convergent responses across models. A consistent activation of the PI3K-Akt signaling pathway was observed, along with modulation of noncanonical NF-κB components such as RELB and CXCL2. TMZ promoted metabolic reprogramming, including SIRT3 upregulation and glycolysis inhibition, and selectively regulated extracellular matrix remodeling genes. Importantly, pro-angiogenic and anti-inflammatory signatures emerged independently of VEGF, with notable downregulation of PTGS2 and TLR4.
conclusionThese results highlight TMZ's potential to modulate gene networks associated with angiogenesis, inflammation, and metabolism. The findings are exploratory and warrant validation in preclinical models to assess their therapeutic relevance.
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