Evidence map›Paper›PMID 27256588›Full record

ArticleScientific reports2016

An isoform of Nedd4-2 is critically involved in the renal adaptation to high salt intake in mice.

Shintaro Minegishi, Tomoaki Ishigami, Tabito Kino, Lin Chen, Rie Nakashima-Sasaki, Naomi Araki, Keisuke Yatsu, Megumi Fujita, Satoshi Umemura

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.5field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Early Enhanced Leucine-RichBioMed research international · 2018
    Article
  12. Article
  13. Article
  14. Eplerenone-Resistant Salt-Sensitive Hypertension in Nedd4-2 C2 KO Mice.International journal of molecular sciences · 2017
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Shintaro MinegishiYokohama City University Graduate School of Medicine, Department of Medical Science and Cardio-Renal Medicine.
Tomoaki IshigamiYokohama City University Graduate School of Medicine, Department of Medical Science and Cardio-Renal Medicine.
Tabito KinoYokohama City University Graduate School of Medicine, Department of Medical Science and Cardio-Renal Medicine.
Lin ChenYokohama City University Graduate School of Medicine, Department of Medical Science and Cardio-Renal Medicine.
Rie Nakashima-SasakiYokohama City University Graduate School of Medicine, Department of Medical Science and Cardio-Renal Medicine.
Naomi ArakiYokohama City University Graduate School of Medicine, Department of Medical Science and Cardio-Renal Medicine.
Keisuke YatsuYokohama City University Graduate School of Medicine, Department of Medical Science and Cardio-Renal Medicine.
Megumi FujitaYokohama City University Graduate School of Medicine, Department of Medical Science and Cardio-Renal Medicine.
Satoshi UmemuraYokohama City University Graduate School of Medicine, Department of Medical Science and Cardio-Renal Medicine.
Yokohama City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial sodium channels (ENaCs) play critical roles in the maintenance of fluid and electrolyte homeostasis, and their genetic abnormalities cause one type of hereditary salt-sensitive hypertension, Liddle syndrome. As we reported previously, both human and rodent Nedd4L/Nedd4-2 showed molecular diversity, with and without a C2 domain in their N-terminal. Nedd4L/Nedd4-2 isoforms with a C2 domain are hypothesized to be related closely to ubiquitination of ENaCs. We generated Nedd4-2 C2 domain knockout mice. We demonstrate here that loss of Nedd4-2 C2 isoform causes salt-sensitive hypertension under conditions of a high dietary salt intake in vivo. The knockout mice had reduced urinary sodium excretion, osmotic pressure and increased water intake and urine volume with marked dilatation of cortical tubules while receiving a high salt diet. To the contrary, there was no difference in metabolic data between wild-type and knockout mice receiving a normal control diet. In the absence of Nedd4-2 C2 domain, a high salt intake accelerated ENaC expression. Coimmunoprecipitation studies revealed suppressed ubiquitination for ENaC with a high salt intake. Taken together, our findings demonstrate that during a high oral salt intake the Nedd4-2 C2 protein plays a pivotal role in maintaining adaptive salt handling in the kidney.

Indexed as

Adaptation, PhysiologicalAnimalsEpithelial Sodium ChannelsHumansHypertensionKidneyMiceMice, KnockoutNedd4 Ubiquitin Protein LigasesProtein IsoformsSodium Chloride, DietaryUbiquitinationEpithelial Sodium ChannelsNedd4l protein, mouseNedd4 Ubiquitin Protein LigasesProtein IsoformsSodium Chloride, Dietary

Identifiers

PMID27256588
PMCPMC4891730
OpenAlexW2412764356

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.