The American journal of the medical sciences
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Secondary hyperparathyroidism, a condition of excess parathyroid hormone (PTH, Pth) production, is often seen in chronic kidney disease (CKD) patients with elevated fibroblast growth factor 23 (FGF23, Fgf23). Elevated FGF23 levels stimulate secondary hyperparathyroidism-associated parathyroid αKlotho signaling. As overexpression of rationally selected microRNAs can suppress target gene activation, we hypothesized that microRNA-based suppression of parathyroid FGF23/αKlotho axis activity may be a potential strategy to combat secondary hyperparathyroidism. ⋯ miR-129 negatively regulates pro-proliferative, Pth-inducing Fgf23/αKlotho signaling in the parathyroid glands of CKD mice.
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Letter Case Reports
Cutaneous Manifestations in Homozygous Familial Hypercholesterolemia.