Parathyroid Disorders and Treatments

This study shows TMEM174 deficiency shortens lifespan by promoting phosphate-driven vascular calcification through its role in NPT2A regulation.

This study shows high-salt diets increase urinary cortisol and decrease plasma FGF23, revealing a novel endocrine interaction with implications for bone, kidney, and cardiovascular health.

This study shows that accelerated citrate production by osteocytes in CKD mice protects kidney function, suggesting citrate handling as a therapeutic target.

This study examines the behavioral and metabolic effects of PTH in mouse models of hyperparathyroidism, finding sex-specific behavioral changes and metabolic alterations.

This study shows that excess FGF23 drives inflammation in kidney disease models and human data, suggesting it as a therapeutic target.

This study develops a computational model of blood pressure regulation and calcium-magnesium homeostasis in rats, showing how disruptions in these systems affect each other and contribute to hypertension and hyperparathyroidism.

This study shows a Western high-phosphate diet worsens CKD-MBD features in Alport Syndrome mice, increasing PTH and FGF23 while reducing klotho, but does not induce vascular calcification.

This study shows targeted chelation therapy with EDTA-NP reduces senescent cells and NLRP3 expression in calcified aortas of CKD models.

This study shows that knocking out Pth4 in zebrafish causes calcium-phosphate imbalance, skeletal issues, and changes in kidney gene expression.

This study shows that combining T3 and baicalein increases Klotho levels in CKD mice, reducing fibrosis and complications like cardiovascular issues and dyslipidemia.

This study identifies mitochondrial dysfunction and impaired mitophagy in CKD-MBD as contributors to renal osteodystrophy, showing reversible effects with rapamycin treatment.

This study identifies structural elements of RGS14 that regulate hormone-sensitive phosphate transport by NPT2A, showing that phosphorylation in the linker and an intact PDZ ligand are essential.

This study uses CRISPR to mutate vitamin D response elements in the Cyp24a1 gene in mice to investigate their role in gene regulation by 1,25(OH)2D3, FGF23, and PTH.

This study investigates the role of Dicer-mediated mTORC1 signaling in parathyroid function using genetic mouse models and clinical data, showing its critical role in maintaining gland integrity and response to CKD.

This study uses single-cell transcriptomics to analyze FGF23 bioactivity and identify novel inflammatory targets in the kidney, revealing interactions between FGF23 and TNF/NF-κB pathways.

This study investigates the role of NRF2 in vascular calcification and aging, finding that NRF2 dysfunction contributes to vascular smooth muscle cell senescence and calcification, with ID2 as a downstream regulator.

This study identifies the subfornical organ (SFO) and paraventricular nucleus (PVN) as central neural regulators of parathyroid hormone (PTH) and bone mass through distinct neuronal subtypes and their interactions.

The paper identifies a pathway where kidney failure induces parathyroid Pin1 phosphorylation, disrupting KSRP activity and increasing PTH mRNA stability, leading to secondary hyperparathyroidism.

This study shows that increased PHOSPHO1 expression in renal osteodystrophy contributes to increased cortical bone mineral density but decreased trabecular bone density.

This study identifies miR-145 and miR-378 as miRNAs that reduce aortic calcification in Klotho mice by repressing BMP signaling.