ArticleClinical kidney journal2015
Calcitonin, the forgotten hormone: does it deserve to be forgotten?
Article in Clinical kidney journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 3 of them syntheses that pooled it.
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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
46 citing papers in PubMed, 3 syntheses or guidelines pooled it, 141 citations in OpenAlex.
- A genome- and phenome-wide association study of plasma procalcitonin concentrations in individuals of European ancestry.EBioMedicine · 2026Pooled it
- Effects of calcium supplementation on the prevention of preeclampsia: an umbrella review of systematic reviews and meta-analyses.Frontiers in medicine · 2025Pooled it
- Pooled it
- Review
- The Pitfalls of Calcitonin as a Tumor Marker: Real-Life Data of Patients with Elevated Basal Calcitonin Levels but Without Evidence of Medullary Thyroid Carcinoma.Journal of clinical medicine · 2026Article
- Degradation of the Molecular Basis of Life During the Aging Process.International journal of molecular sciences · 2026Review
- Natural product-based interventions for thyroid disorders: mechanisms and applications.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Epidemiological relevant effect biomarkers for thyroid hormone system related adverse outcome pathways: a literature review.Frontiers in pharmacology · 2026Review
- The interrelationship between calcium-phosphorus homeostasis and bone remodelling. Impact of dietary changes on bone in patients with primary hyperparathyroidism and chronic kidney disease.Frontiers in bioengineering and biotechnology · 2026Article
- Biomolecular Basis of Life.Metabolites · 2025Review
- Article
- Lactylation's role in bone health and disease: mechanistic insights and therapeutic potential.PeerJ · 2025Review
- Effect of birth type and sex on growth performance, wither height, humerus-radius bone dimensions, humerus-ulna growth plate width and selected hormone profile in growing Gurcu goat kids.Veterinary medicine and science · 2024Article
- Blood biomarkers for occupational hand-arm vibration exposure.Toxicology and industrial health · 2024Article
- Peptide Drugs: Current Status and it's Applications in the Treatment of Various Diseases.Current drug research reviews · 2024Review
- Exploring the relationship between calcitonin, ionized calcium, and bone turnover in cats with and without naturally occurring hypercalcemia.Frontiers in veterinary science · 2024Article
- Article
- Structural and Metabolic Changes in Bone.Animals : an open access journal from MDPI · 2022Review
- Parathyroid hormone and calcitonin response during the calcium infusion test in patients with primary hyperparathyroidism.Hormones (Athens, Greece) · 2022Article
- A Retrospective Study of Serum Calcium Status in Tehran, Iran (105,128 Samples, from 2009-2018).Iranian journal of public health · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcitonin is a 32 amino acid hormone secreted by the C-cells of the thyroid gland. Calcitonin has been preserved during the transition from ocean-based life to land dwellers and is phylogenetically older than parathyroid hormone. Calcitonin secretion is stimulated by increases in the serum calcium concentration and calcitonin protects against the development of hypercalcemia. Calcitonin is also stimulated by gastrointestinal hormones such as gastrin. This has led to the unproven hypothesis that postprandial calcitonin stimulation could play a role in the deposition of calcium and phosphate in bone after feeding. However, no bone or other abnormalities have been described in states of calcitonin deficiency or excess except for diarrhea in a few patients with medullary thyroid carcinoma. Calcitonin is known to stimulate renal 1,25 (OH)2 vitamin D (1,25D) production at a site in the proximal tubule different from parathyroid hormone and hypophosphatemia. During pregnancy and lactation, both calcitonin and 1,25D are increased. The increases in calcitonin and 1,25D may be important in the transfer of maternal calcium to the fetus/infant and in the prevention and recovery of maternal bone loss. Calcitonin has an immediate effect on decreasing osteoclast activity and has been used for treatment of hypercalcemia. Recent studies in the calcitonin gene knockout mouse have shown increases in bone mass and bone formation. This last result together with the presence of calcitonin receptors on the osteocyte suggests that calcitonin could possibly affect osteocyte products which affect bone formation. In summary, a precise role for calcitonin remains elusive more than 50 years after its discovery.
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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.