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Updated: Jul 15, 2026

Generation of Hypoparathyroid Rats via Carbon-Nanoparticle-Assisted Parathyroidectomy
Published on: July 14, 2023
[The mechanisms of parathyroid hyperplasia and its regression]
Masanori Tokumoto1, Masatomo Taniguchi
1Washington University School of Medicine, Department of Internal Medicine, Renal Division, USA.
Abstract:
Parathyroid gland (PTG) is a unique endocrine organ in which the quiescent glandular cells begin to proliferate in the progressive course of renal failure, leading to secondary hypereparathyroidism (SHPT). SHPT is characterized by continuous over-secretion of parathyroid hormone (PTH) and parathyroid hyperplasia, and the major contributing factors are a deficiency of active vitamin D, hypocalcemia and phosphate retention. Many experimental and human studies have revealed that the down-regulations of vitamin D receptor (VDR), calcium (Ca) -sensing receptor (CaSR), and retinoid X receptor (RXR) in parathyroid hyperplasia of SHPT, especially nodular hyperplasia, which is a severe form of hyperplasia. These also contribute to progression of parathyroid hyperplasia. Recently, mechanisms by which active vitamin D and Ca regulate parathyroid hyperplasia via their receptors have been clarified. In this paper, we review mechanisms for progression of parathyroid hyperplasia and the possibility for regression of parathyroid hyperplasia.
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