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In physiological wound healing, the temporary upregulation of TGF-β induces NR4A1 expression creating a negative feedback loop, while the persistent activation of TGF-β signalling in fibrotic diseases uses protein kinase B (PKB), also known as AKT, and histone deacetylase-dependent mechanisms to inhibit NR4A1 expression and activation [17]

Sodium Chloride

Strength:3ml

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