Evidence map›Paper›PMID 41498836›Full record

ReviewPurinergic signalling2026

Current understanding of ENaC regulation by P2Y2/PLC/PI(4,5)P2 pathway.

Tarek Mohamed Abd El-Aziz, Ahmed Al-Sabi, Lucia A Seale, Antonio G Soares

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Purinergic signalling, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

4 authors.

Tarek Mohamed Abd El-AzizZoology Department, Faculty of Science, Minia University, El-Minia, Egypt.
Ahmed Al-SabiCollege of Integrative Studies, Abdullah Al Salem University, Khaldiya, Kuwait.
Lucia A SealePacific Biosciences Research Center, University of Hawai'i at Mānoa, Honolulu, HI, USA.
Antonio G SoaresPacific Biosciences Research Center, University of Hawai'i at Mānoa, Honolulu, HI, USA. agsj@hawaii.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The epithelial sodium channel (ENaC) localized in the cell membrane is crucial for sodium transport and blood pressure regulation. Discovered in frog skin, ENaC is expressed in the colon, lungs, exocrine glands, and most notably in the distal nephron of the kidneys, where it limits sodium reabsorption. Mutations in ENaC cause hereditary hypertension (Liddle's syndrome) or hypotension (pseudohypoaldosteronism type 1). ENaC activity and expression are tightly controlled by various signaling molecules and second messengers. For example, urinary ATP binding to the P2Y2 receptor inhibits ENaC. ENaC also interacts with PI(4,5)P2 and the ubiquitin ligase Nedd4-2 via specific motifs. PI(4,5)P2 is essential for ENaC stability, trafficking, and gating. This review focuses on the regulatory roles of the P2Y2 receptor and PI(4,5)P2 on ENaC regulation.

Indexed as

Epithelial Sodium ChannelsReceptors, Purinergic P2Y2Signal TransductionType C PhospholipasesAnimalsHumansEpithelial Sodium ChannelsReceptors, Purinergic P2Y2Type C PhospholipasesEpithelial sodium channelPhospholipidsPurinergic receptor

Identifiers

PMID41498836
PMCPMC12779786

What OpenQuestion holds

Textmetadata
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.