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These physiological consequences may serve as important explanations for the rise in VO2max [147, 148]

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While recent research has markedly enriched our understanding regarding the association between elevated UA and the risk of CVD and the underlying mechanisms of the association, so far it failed to offer a clear answer to the causality in the relationship between UA and CVD

Similarly, inhibition of LOX15 ameliorated AA-induced LPO (Supplementary Fig

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