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It has been proposed that the pathophysiology of IIM could be attributed to increased cell death, inadequate removal of cell debris, and excessive autoantigens and pro-inflammatory cytokines, which eventually result in over-stimulated immunological and inflammatory responses (152)

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However, significant challenges remain, including the synthesis of stable tripeptides with good tissue penetration, insufficient understanding of their mechanisms of action, the scarcity of studies in larger animal models and human trials, and the lack of direct head-to-head comparisons with larger peptides [75, 95]