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Secondary mechanisms include modulation of inflammatory cytokines and interaction with growth factor receptors, contributing to its broad regenerative profile in research models focused on musculoskeletal, gastrointestinal, and neural tissues

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10.1016/j.carbpol.2014.12.084 38

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First, most mechanistic evidence is derived from viral myocarditis or experimental autoimmune myocarditis models, which capture specific inflammatory contexts but do not fully reflect the heterogeneity of human myocarditis