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To understand the underlying mechanisms, inhibitors targeting the Notch pathway (DAPT) and NF-B pathway (BMS) were also applied to HUVEC and murine CLI models

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This mechanism involves: Sequestration of monomeric actin (G-actin) to prevent premature polymerization Promotion of actin polymerization into functional microfilaments (F-actin) when needed Enhanced cellular migration through cytoskeletal reorganization Facilitation of cell shape changes necessary for wound healing Research indicates TB-500 may work with the Arp2/3 protein complex to orchestrate actin polymerization, though this mechanism requires further clarification[4]

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