ReviewEndocrine pathology2004
Calcium sensing by endocrine cells.
Review in Endocrine pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.
- Graves' disease and bone mineral density: a meta-analysis and UK Biobank.Frontiers in endocrinology · 2026Pooled it
- A cell function study on calcium regulation of a novel calcium-sensing receptor mutation (p.Tyr825Phe).Annals of pediatric endocrinology & metabolism · 2021Article
- The full-length calcium-sensing receptor dampens the calcemic response to 1alpha,25(OH)2 vitamin D3 in vivo independently of parathyroid hormone.American journal of physiology. Renal physiology · 2009Article
- Hypercalcaemic and hypocalcaemic conditions due to calcium-sensing receptor mutations.Best practice & research. Clinical rheumatology · 2008Review
- Extracellular calcium as an integrator of tissue function.The international journal of biochemistry & cell biology · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The elucidation of the structure and function of the Ca2+(o)-sensing receptor (CaR) has provided important insights into the normal control of Ca2+(o) homeostasis, particularly the key role of the receptor in kidney and parathyroid. Further studies are needed to define more clearly the homeostatic role of the CaR in additional tissues, both those that are involved and those that are uninvolved in systemic Ca2+(o) homeostasis. The availability of the cloned CaR has also permitted documentation of the molecular basis of inherited disorders of Ca2+(o) sensing, including those in which the receptor is less and or more sensitive than normal to Ca2+(o). Antibodies to the CaR that either activate it or inactivate it produce syndromes resembling the corresponding genetic diseases. Expression of the receptor is abnormally low in 1 degree and 2 degrees hyperparathyroidism, which could contribute to the defective Ca2+(o) sensing in these conditions. The recent discovery of calcimimetics, which sensitize the CaR to Ca2+(o), has provided what will likely be an effective medical therapy for the secondary/tertiary hyperparathyroidism of end stage renal failure as well as for 1 degree hyperparathyroidism.
Indexed as
Identifiers
What OpenQuestion holds
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.