ArticleAmerican journal of physiology. Renal physiology2013
Activation of the Ca(2+)-sensing receptor increases renal claudin-14 expression and urinary Ca(2+) excretion.
Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 120 citations in OpenAlex.
- Disruption of Claudin-2 and Trpv6 Results in Hypocalcemia, Hypercalciuria, and Altered Bone Microarchitecture in Mice.Acta physiologica (Oxford, England) · 2026Article
- Endocrine regulation of uromodulin in aging.Frontiers in endocrinology · 2026Review
- Control of renal calcium permeability via a tight junctional claudin switch.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Hypercalcemia's Hidden Regulator: Calcium-Sensing Receptor and the Kidney's Secret Weapon.Journal of the American Society of Nephrology : JASN · 2025Article
- Calcium-Sensing Receptor in the Thick Ascending Limb and Renal Response to Hypercalcemia.Journal of the American Society of Nephrology : JASN · 2025Article
- Biology of calcium homeostasis regulation in intestine and kidney.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025Review
- Ion permeability profiles of renal paracellular channel-forming claudins.Acta physiologica (Oxford, England) · 2025Article
- Paracellular Transport and Renal Tubule Calcium Handling: Emerging Roles in Kidney Stone Disease.Journal of the American Society of Nephrology : JASN · 2024Review
- Disruption of the c-terminal serine protease domain of Fam111a does not alter calcium homeostasis in mice.Physiological reports · 2024Article
- Claudin-10 Expression and the Gene Expression Pattern of Thick Ascending Limb Cells.International journal of molecular sciences · 2024Article
- Calcium sensing receptor regulate claudin-14 via PKA-STAT3 pathway in rat model of nephrolithiasis.Frontiers in pharmacology · 2024Article
- Preliminary study of the role of nanobacteria in the formation of renal stones in experimental rats and its mechanism.Archives of medical sciences. Atherosclerotic diseases · 2024Article
- Contribution of thick ascending limb and distal convoluted tubule to glucose-induced hypercalciuria in healthy controls.American journal of physiology. Renal physiology · 2023Article
- Expression of phosphate and calcium transporters and their regulators in parotid glands of mice.Pflugers Archiv : European journal of physiology · 2023Article
- The importance of kidney calcium handling in the homeostasis of extracellular fluid calcium.Pflugers Archiv : European journal of physiology · 2022Review
- Regulation of 1 and 24 hydroxylation of vitamin D metabolites in the proximal tubule.Experimental biology and medicine (Maywood, N.J.) · 2022Review
- Claudins in kidney health and disease.Kidney research and clinical practice · 2022Article
- Pathophysiological aspects of the thick ascending limb and novel genetic defects: HELIX syndrome and transient antenatal Bartter syndrome.Pediatric nephrology (Berlin, Germany) · 2022Review
- A Genetic Polymorphism in theFrontiers in genetics · 2022Article
- Calcium sensitive receptor and claudin-14 expression in kidney tissues of two kidney stone models.Archives of medical science : AMS · 2022Article
1 more citing papers are in PubMed but not listed here.
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6 authors at 1 institution in 1 country.
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Abstract
Kidney stones are a prevalent clinical condition imposing a large economic burden on the healthcare system. Hypercalciuria remains the major risk factor for development of a Ca(2+)-containing stone. The kidney's ability to alter Ca(2+) excretion in response to changes in serum Ca(2+) is in part mediated by the Ca(2+)-sensing receptor (CaSR). Recent studies revealed renal claudin-14 (Cldn14) expression localized to the thick ascending limb (TAL) and its expression to be regulated via the CaSR. We find that Cldn14 expression is increased by high dietary Ca(2+) intake and by elevated serum Ca(2+) levels induced by prolonged 1,25-dihydroxyvitamin D3 administration. Consistent with this, activation of the CaSR in vivo via administration of the calcimimetic cinacalcet hydrochloride led to a 40-fold increase in Cldn14 mRNA. Moreover, overexpression of Cldn14 in two separate cell culture models decreased paracellular Ca(2+) flux by preferentially decreasing cation permeability, thereby increasing transepithelial resistance. These data support the existence of a mechanism whereby activation of the CaSR in the TAL increases Cldn14 expression, which in turn blocks the paracellular reabsorption of Ca(2+). This molecular mechanism likely facilitates renal Ca(2+) losses in response to elevated serum Ca(2+). Moreover, dysregulation of the newly described CaSR-Cldn14 axis likely contributes to the development of hypercalciuria and kidney stones.
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