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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

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The result, for many people, is a chronic lower-level insufficiency that does not produce clinical deficiency symptoms but nonetheless affects the quality of immune response, skin health, collagen production and overall cellular resilience

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