The roles of mTORC1 in parathyroid gland function in chronic kidney disease-induced secondary hyperparathyroidism: Evidence from male genetic mouse models and clinical data.

ABSTRACT: Secondary hyperparathyroidism (SHP) associated with chronic kidney disease (CKD) contributes to morbidity and mortality, yet the related parathyroid signaling pathways are not fully understood. Previous studies have indicated that the parathyroid mTORC1 pathway is activated in both experimental CKD and hypocalcemia-induced SHP. Furthermore, mice with parathyroid-specific mTOR deficiency (PT-mTOR^-/-) exhibit disrupted parathyroid glands, but maintain normal serum PTH levels. Conversely, PT-Tsc1^-/- mice, with mTORC1 hyperactivation, have enlarged glands and high serum PTH and calcium levels. We now uncover links between mTORC1 function, parathyroid gland morphology, and the response to CKD. Despite impaired gland structure, PT-mTOR^-/- mice increased serum PTH

SUBMITTER: Khalaily N 

PROVIDER: S-EPMC11580712 | biostudies-literature | 2024 Nov

REPOSITORIES: biostudies-literature