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Myotendinous Junction Repair (Japjec et al., 2021) In myotendinous-junction injuries, BPC-157 led to full defect closure and functional restoration within six weeks, normalizing nitric-oxide pathways and revascularization

Morphologically, ferroptosis primarily exhibits a necrotic phenotype, with mitochondrial alterations being dominant, such as significant mitochondrial shrinkage, increased membrane density, and reduction or loss of mitochondrial cristae and outer membranes [20]

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