Increased Levels of BAMBI Inhibit Canonical TGF-β Signaling in Chronic Wound Tissues

Chronic wounds affect more than 2% of the population worldwide, with a significant burden on affected individuals, healthcare systems, and societies. A key regulator entire wound healing cascade is transforming growth factor beta (TGF-β), which regulates not only inflammation extracellular matrix formation but also revascularization. This present work aimed at characterizing tissues obtained from acute chronic regarding angiogenesis, inflammation, as well ECM degradation, to identify common disturbances in process. Serum 38 patients (N = 20 N 18 wounds) were analyzed. The patients’ sera suggested shift VEGF/VEGFR ANGPT/TIE2 signaling wounds. However, this was confirmed tissues. Instead, showed increased levels MMP9, known activator TGF-β. regulation TGF-β target genes, such CTGF, COL1A1, or IL-6, absent In tissues, all three isoforms expressed TGF-β1 TGF-β3 reporter assay that activated. Western blots immunostaining decreased canonical respective suggesting presence inhibitor. As potential regulatory mechanism, proteome profiler array elevated pseudo-receptor BAMBI. Also, tissue expression BAMBI significantly (10.6-fold) had become (9.5-fold). summary, our data indicate possible role development available few vivo studies support findings by postulating therapeutic for controlling scar formation.