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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

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coli w3110 strain, which initially undergone multiple random mutagenesis and then overexpressing aroF WT and pheA fbr based on system-wide analysis of metabolism results in gradual increase in L-phenylalanine production throughout the strain engineering steps 27

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