ArticleJournal of molecular medicine (Berlin, Germany)2013
The chloride channel/transporter Slc26a9 regulates the systemic arterial pressure and renal chloride excretion.
Article in Journal of molecular medicine (Berlin, Germany), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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
21 citing papers in PubMed, 35 citations in OpenAlex.
- Diet-Microbiota-Host Interactions in Regulation of Cardiometabolic Homeostasis: Emerging Mechanisms and Therapeutic Potential.Microbiota and host · 2025Article
- Chloride/Multiple Anion Exchanger SLC26A Family: Systemic Roles of SLC26A4 in Various Organs.International journal of molecular sciences · 2024Review
- SLC26A9 promotes colorectal tumorigenesis by modulating Wnt/β-catenin signaling.Cell death discovery · 2024Article
- SLC26 Anion Transporters.Handbook of experimental pharmacology · 2024Review
- Identification of candidate biomarkers and pathways associated with type 1 diabetes mellitus using bioinformatics analysis.Scientific reports · 2022Article
- Expression of SLC26A9 in Airways and Its Potential Role in Asthma.International journal of molecular sciences · 2022Article
- SLC26A9 as a Potential Modifier and Therapeutic Target in Cystic Fibrosis Lung Disease.Biomolecules · 2022Review
- Article
- Increased expression of anion transporter SLC26A9 delays diabetes onset in cystic fibrosis.The Journal of clinical investigation · 2020Article
- Structural insights into the gating mechanism of human SLC26A9 mediated by its C-terminal sequence.Cell discovery · 2020Article
- Genetic association and transcriptome integration identify contributing genes and tissues at cystic fibrosis modifier loci.PLoS genetics · 2019Article
- Physiological and Pathophysiological Relevance of the Anion Transporter Slc26a9 in Multiple Organs.Frontiers in physiology · 2018Review
- Chloride Homeostasis in Neurons With Special Emphasis on the Olivocerebellar System: Differential Roles for Transporters and Channels.Frontiers in cellular neuroscience · 2018Review
- The CFTR trafficking mutation F508del inhibits the constitutive activity of SLC26A9.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- The non-diuretic hypotensive effects of thiazides are enhanced during volume depletion states.PloS one · 2017Article
- The multiple roles of pendrin in the kidney.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2015Review
- Loss of Slc26a9 anion transporter alters intestinal electrolyte and HCO3(-) transport and reduces survival in CFTR-deficient mice.Pflugers Archiv : European journal of physiology · 2015Article
- Novel Roles for Chloride Channels, Exchangers, and Regulators in Chronic Inflammatory Airway Diseases.Mediators of inflammation · 2015Review
- Disturbed acid-base transport: an emerging cause of hypertension.Frontiers in physiology · 2013Review
- SLC26 Cl-/HCO3- exchangers in the kidney: roles in health and disease.Kidney international · 2013Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Apical chloride secretory pathways in the kidney medullary collecting duct are thought to play an important role in the modulation of final urine composition and regulation of systemic vascular volume and/or blood pressure. However, the molecular identity of these molecules has largely remained unknown. Here, we demonstrate that Slc26a9, an electrogenic chloride channel/transporter, is localized on the apical membrane of principal cells in the kidney medullary collecting duct and mediates chloride secretion. Mice with the genetic deletion of Slc26a9 show significant reduction in renal chloride excretion when fed a diet high in salt or subjected to water deprivation. Arterial pressure measurements indicated that Slc26a9 knockout (Slc26a9(-/-)) mice are hypertensive under baseline conditions and increase their blood pressure further within 48 h of switching to a high-salt diet. These results suggest that Slc26a9 plays an important role in renal chloride/fluid excretion and arterial pressure regulation. We propose that impaired SLC26A9 activity in humans may interfere with the excretion of excess salt and result in hypertension.
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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.