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These risks arise through direct or indirect interactions with cellular systems, which may disrupt homeostasis, trigger oxidative stress, and dysregulate critical molecular pathways that can culminate in organ toxicity or metabolic dysfunction
SS26
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In particular, in both muscle (transected or crushed) and transected tendon healing, we noted an increase in early angiogenesis (and the increased expression of VEGF, Factor VIII, and CD34), while late angiogenesis decreased (and the expression of VEGF, Factor VIII, and CD34 was decreased)[3]
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