ArticleScience translational medicine2015
Sodium channel Nax is a regulator in epithelial sodium homeostasis.
Article in Science translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 71 citations in OpenAlex.
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- Implications of pH and Ionic Environment in Chronic Diabetic Wounds: An Overlooked Perspective.Clinical, cosmetic and investigational dermatology · 2024Review
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- Chitosan-Glycolic Acid Gel Modification of Chloride Ion Transport in Mammalian Skin: An In Vitro Study.Molecules (Basel, Switzerland) · 2023Article
- Serine protease 35 regulates the fibroblast matrisome in response to hyperosmotic stress.Science advances · 2023Article
- Nickel ions influence the transepithelial sodium transport in the trachea, intestine and skin.Scientific reports · 2023Article
- The Impact of Diclofenac Gel on Ion Transport in the Rabbit (Molecules (Basel, Switzerland) · 2023Article
- Bioelectric Signaling: Role of Bioelectricity in Directional Cell Migration in Wound Healing.Cold Spring Harbor perspectives in biology · 2022Review
- Structure-guided unlocking of NaNature communications · 2022Article
- Identification of SCN7A as the key gene associated with tumor mutation burden in gastric cancer.BMC gastroenterology · 2022Article
- Inhibition of Severe Acute Respiratory Syndrome Coronavirus 2 Replication by Hypertonic Saline Solution in Lung and Kidney Epithelial Cells.ACS pharmacology & translational science · 2021Article
- Review
- NaHeliyon · 2021Article
Corrections and comments
- Commented on byNa2016
Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms by which the epidermis responds to disturbances in barrier function and restores homeostasis are unknown. With a perturbation of the epidermal barrier, water is lost, resulting in an increase in extracellular sodium concentration. We demonstrate that the sodium channel Nax functions as a sodium sensor. With increased extracellular sodium, Nax up-regulates prostasin, which results in activation of the sodium channel ENaC, resulting in increased sodium flux and increased downstream mRNA synthesis of inflammatory mediators. Nax is present in multiple epithelial tissues, and up-regulation of its downstream genes is found in hypertrophic scars. In animal models, blocking Nax expression results in improvement in scarring and atopic dermatitis-like symptoms, both of which are pathological conditions characterized by perturbations in barrier function. These findings support an important role for Nax in maintaining epithelial homeostasis.
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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.