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For example, i) most mechanistic insights are derived from preclinical models, and direct clinical evidence linking platelet mitochondrial modulation to improved cardiovascular outcomes is limited, ii) antidiabetic agents such as metformin exhibit dose- and context-dependent effects on platelet mitochondria, which remain incompletely understood, iii) the effects of metabolic status, drug interactions, and disease stage on platelet mitochondrial function have not been systematically evaluated, iv) translation of mitochondrial-targeted antioxidants and mitochondrial transplantation is further constrained by unresolved issues related to delivery, specificity, safety, and long-term efficacy, v) In parallel, nanomedicine-based approaches are emerging as innovative strategies to target platelet dysfunction with enhanced precision