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(49) have confirmed that in vitro treatment with UA can reduce the expression levels of fibrosis markers including vimentin, discoidin domain receptor tyrosine kinase 2, tensin and Alpha-smooth muscle actin in myocardial tissues, and inhibit the transition of cardiac fibroblasts to a fibrotic state through nuclear factor erythroid 2-related factor 2 signaling pathway

In the reduced state, the thiol group of cysteinyl residue is a source of one reducing equivalent

This medication may interfere with certain laboratory tests (including parathyroid function), possibly causing false test results

Phosphodiesterase-5 (PDE5) inhibitors remain the first-line pharmacological treatment for ED according to NICE guidance