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Thus, TB-500 may be hypothesized to support angiogenesis by combining a cytoskeleton-linked increase in endothelial motility with signaling changes that raise pro-angiogenic programs (VEGF-A and Ang2/Tie2) via Notch/NF-B coupling in damaged cellular structure

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In summary, SLC7A5 overexpression was able to reverse the protective effects of YTHDF1 knockdown, revealing the critical role of SLC7A5 in the YTHDF1-mediated cytoprotective mechanism

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