ArticleUrological research2008
Enteric oxalate secretion is not directly mediated by the human CFTR chloride channel.
Article in Urological research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Oxalate secretion is stimulated by a cAMP-dependent pathway in the mouse cecum.Pflugers Archiv : European journal of physiology · 2023Article
- The role of NHE3 (Slc9a3) in oxalate and sodium transport by mouse intestine and regulation by cAMP.Physiological reports · 2021Article
- Absence of the sulfate transporter SAT-1 has no impact on oxalate handling by mouse intestine and does not cause hyperoxaluria or hyperoxalemia.American journal of physiology. Gastrointestinal and liver physiology · 2019Article
- The role of intestinal oxalate transport in hyperoxaluria and the formation of kidney stones in animals and man.Urolithiasis · 2017Review
- Loss of Cystic Fibrosis Transmembrane Regulator Impairs Intestinal Oxalate Secretion.Journal of the American Society of Nephrology : JASN · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The secretion of the oxalate anion by intestinal epithelia is a functionally significant component of oxalate homeostasis and hence a relevant factor in the etiology and management of calcium oxalate urolithiasis. To test the hypothesis that human cystic fibrosis transmembrane conductance regulator (hCFTR) can directly mediate the efflux of the oxalate anion, we compared cAMP-stimulated 36Cl-, 14C-oxalate, and 35SO(4)2- efflux from Xenopus oocytes expressing hCFTR with water-injected control oocytes. hCFTR-expressing oocytes exhibited a large, reversible cAMP-dependent increase in whole cell conductance measured using a two-electrode voltage clamp and a 13-fold increase in rate of cAMP-stimulated 36Cl- efflux. In contrast, the rate constants of oxalate and sulfate efflux were low and unaffected by cAMP in either control or hCFTR-expressing oocytes. We conclude that the human CFTR gene product does not directly mediate oxalate efflux in secretory epithelia and hence is not directly involved in oxalate homeostasis in humans.
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Registered trials
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