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Many cardiovascular risk factors such as diabetes mellitus, hypertension and hyperlipidemia are demonstrated to stimulate the interaction of Cav-1 and eNOS, reduce nitric oxide production resulting in endothelial dysfunction and subsequently the formation of atherosclerotic lesion 41,42,43

This approach prioritizes consistency and comprehensive pathway coverage

Second, many available studies are characterized by small sample sizes or lack appropriate control groups, making it difficult to draw definitive conclusions about therapeutic efficacy and optimal treatment protocols

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