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Wound Healing & Tissue Regeneration Research Clinical validation demonstrates accelerated wound closure rates exceeding 60% compared to controls across multiple injury models including chemical burns, surgical wounds, and chronic ulcers
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It also promotes apoptosis through upregulation of p53-dependent pathways and cell cycle arrest at G1 phase, mediated by modulation of key downstream targets, such as FoxO1, miR-215, miR-96, CD44, survivin, and VEGF, thereby limiting tumor survival and metastasis 165