Evidence map›Paper›PMID 19996890›Full record

ReviewCurrent opinion in nephrology and hypertension2010

Regulation of sodium transport by ENaC in the kidney.

L Lee Hamm, Zhuang Feng, Kathleen S Hering-Smith

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in nephrology and hypertension, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

41 citing papers in PubMed, 90 citations in OpenAlex.

  1. Article
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  3. The scaffold protein IQGAP1 regulates the epithelial NaThe Journal of biological chemistry · 2025
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  16. Greater natriuretic response to ENaC inhibition in male versus female Sprague-Dawley rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2020
    Article
  17. Article
  18. Article
  19. Net KKidney international · 2017
    Article
  20. 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

3 authors at 2 institutions in 1 country.

L Lee HammDepartments of Medicine, Physiology and the Tulane Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana 70112, USA. Lhamm@tulane.edu
Zhuang Feng
Kathleen S Hering-Smith
Southeast Louisiana Veterans Health Care System · USTulane University · US

Funding

Tulane NPRC SPF Sheltered Outdoor Enclosure ExpansionP51OD011104 · OD · TULANE UNIVERSITY OF LOUISIANA · PI L Lee HAMM · 2012 to 2026
$142.4M
TULANE COBRE: TRANSGENIC &GENE-TARGETED ANIMAL COREP20RR017659 · NCRR · TULANE UNIVERSITY OF LOUISIANA · PI PRIETO, MINOLFA C · 2002 to 2011
$22.1M
REGULATION OF CITRATE TRANSPORTR01DK054952 · NIDDK · TULANE UNIVERSITY OF LOUISIANA · PI HAMM, LEE · 2000 to 2003
$794k
NCRR NIH HHS P20 RR017659NCRR NIH HHS P20RR017659NIDDK NIH HHS R01 DK054952NIH HHS P51 OD011104
6 · The paper itself

Abstract

purpose of reviewThe amiloride-sensitive epithelial sodium channel (ENaC) plays a major role in the regulation of sodium transport in the collecting duct and hence sodium balance. This review describes recent findings in the regulation of ENaC function by serine proteases in particular and other regulatory aspects. RECENT

findingsRegulation of ENaC occurs at many levels (biophysical, transcriptional, post-translational modifications, assembly, membrane insertion, retrieval, recycling, degradation, etc.). Recent studies have recognized and delineated proteolytic cleavage, particularly of the alpha and gamma subunits, as major mechanisms of activation. Release of peptide fragments from these two subunits appears to be an important aspect of activation. These proteolytic mechanisms of ENaC activation have also been demonstrated in vivo and strongly suggested in clinical circumstances, particularly the nephrotic syndrome. In the nephrotic syndrome, filtered plasminogen may be cleaved by tubular urokinase to yield plasmin which can activate ENaC. In addition to these mechanisms, regulation by ubiquitination and deubiquitination represents a pivotal process. Several important deubiquitinating enzymes have been identified as important in ENaC retention in, or recycling to, the apical membrane. New aspects of the genomic control of ENaC transcription have also been found including histone methylation. SUMMARY: The mechanisms of regulation of ENaC are increasingly understood to be a complex interplay of many different levels and systems. Proteolytic cleavage of alpha and gamma subunits plays a major role in ENaC activation. This may be particularly clinically relevant in nephrotic syndrome in which plasmin may activate ENaC activity.

Indexed as

AnimalsEpithelial Sodium ChannelsFibrinolysinHumansIon TransportKidneyModels, BiologicalNephrotic SyndromeProtease InhibitorsProtein SubunitsSerine ProteasesSodiumTransforming Growth Factor beta1Epithelial Sodium ChannelsFibrinolysinProtease InhibitorsProtein SubunitsSerine ProteasesSodiumTransforming Growth Factor beta1

Identifiers

PMID19996890
PMCPMC2895494
OpenAlexW1978529103

What OpenQuestion holds

Textmetadata
LicenceTDM
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.