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Mitochondrial dysfunction in pathophysiology of heart failure

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Experimental research has demonstrated that PCs therapy diminishes the proliferation and migration of human aortic smooth muscle cells (HASMCs) triggered by AGEs by elevating UCH-L1 protein levels, reducing IB- degradation, and curtailing NF-B nuclear translocation in a dose-responsive manner (Qian et al., 2011)

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The bioavailability differs, the dosing schedule changes from weekly to daily, and the evidence base is less robust