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A.et al (2004)

(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

doi: 10.1002/hep.24283 113 LuoFOldoniFDasA

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Understanding how long term care facilities manage patients with comorbid metabolic conditions also influences demand patterns for GLP-1 therapies in institutional care settings