ArticleJournal of the American Society of Nephrology : JASN2011
Cyclooxygenase 2 promotes parathyroid hyperplasia in ESRD.
Article in Journal of the American Society of Nephrology : JASN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 24 citations in OpenAlex.
- Unraveling the mystery of parathyroid oxyphil cells in uremic SHPT: ongoing challenges and multi-omics advances.Journal of molecular cell biology · 2026Review
- Stattic engineering M2 macrophage-derived exosomes mediate autophagy and immune reprogramming for secondary hyperparathyroidism.Journal of advanced research · 2026Article
- Article
- Molecular Mechanisms of Parathyroid Disorders in Chronic Kidney Disease.Metabolites · 2022Review
- Mechanism of calcitriol regulating parathyroid cells in secondary hyperparathyroidism.Frontiers in pharmacology · 2022Review
- Parathyroid Cell Proliferation in Secondary Hyperparathyroidism of Chronic Kidney Disease.International journal of molecular sciences · 2020Review
- Oxylipin profiling of human plasma reflects the renal dysfunction in uremic patients.Metabolomics : Official journal of the Metabolomic Society · 2018Article
- Association of circulating fibroblast growth factor-23 with renal phosphate excretion among hemodialysis patients with residual renal function.Clinical journal of the American Society of Nephrology : CJASN · 2013Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperplasia of the PTG underlies the secondary hyperparathyroidism (SHPT) observed in CKD, but the mechanism underlying this hyperplasia is incompletely understood. Because aberrant cyclooxygenase 2 (COX2) expression promotes epithelial cell proliferation, we examined the effects of COX2 on the parathyroid gland in uremia. In patients with ESRD who underwent parathyroidectomy, clusters of cells within the parathyroid glands had increased COX2 expression. Some COX2-positive cells exhibited two nuclei, consistent with proliferation. Furthermore, nearly 78% of COX2-positive cells expressed proliferating cell nuclear antigen (PCNA). In the 5/6-nephrectomy rat model, rats fed a high-phosphate diet had significantly higher serum PTH levels and larger parathyroid glands than sham-operated rats. Compared with controls, the parathyroid glands of uremic rats exhibited more PCNA-positive cells and greater COX2 expression in the chief cells. Treatment with COX2 inhibitor celecoxib significantly reduced PCNA expression, attenuated serum PTH levels, and reduced the size of the glands. In conclusion, COX2 promotes the pathogenesis of hyperparathyroidism in ESRD, suggesting that inhibiting the COX2 pathway could be a potential therapeutic target.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.