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Copper transport into the nucleus is facilitated by CCS and subsequently mediated by the copper-binding protein (CuBP) (49)

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The mechanisms of renal interstitial fibrosis are generally thought to be related to inflammatory responses, activation and proliferation of fibroblasts, accumulation of extracellular matrix (ECM), epithelial-mesenchymal transition (EMT) (5), agonism of the renin-angiotensin system (RAS) and metabolic abnormalities, for instance, both an excess of parathyroid hormone and a deficiency of vitamin D can contribute to the progression of renal fibrosis in the patients with CKD (2,3,6)