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31,35 In contrast, our results revealed that CPT1A-mediated FAO was a crucial metabolic characteristic of LCSCs, and the suppression of CPT1A promoted ferroptosis sensitivity but not apoptosis in LCSCs

The results suggested that TB-500 not only potentially enhanced the viability, angiogenesis, and migratory ability of HUVEC but possibly also promoted the expression of angiopoietin-2 (Ang2), TEK receptor tyrosine kinase 2 (tie2), vascular endothelial growth factor A (VEGFA), NOTCH1 intracellular domain (N1ICD), Notch receptor 3 (Notch3), NF-B, and phosphorylated (p)-p65 in HUVEC