Evidence map›Paper›PMID 35111062›Full record

ArticleFrontiers in pharmacology2021

Inhibition of the Aquaporin-1 Cation Conductance by Selected Furan Compounds Reduces Red Blood Cell Sickling.

Pak Hin Chow, Charles D Cox, Jinxin V Pei, Nancy Anabaraonye, Saeed Nourmohammadi, Sam W Henderson, Boris Martinac, Osheiza Abdulmalik, Andrea J Yool

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
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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 4 institutions in 2 countries.

Pak Hin ChowAquaporin Physiology and Drug Discovery Program, School of Biomedicine, University of Adelaide, Adelaide, SA, Australia.
Charles D CoxVictor Chang Cardiac Research Institute, Darlinghurst, NSW, Australia.
Jinxin V PeiResearch School of Biology, College of Science, Australian National University, Canberra, ACT, Australia.
Nancy AnabaraonyeDivision of Hematology, Children's Hospital of Philadelphia, Philadelphia, PA, United States.
Saeed NourmohammadiAquaporin Physiology and Drug Discovery Program, School of Biomedicine, University of Adelaide, Adelaide, SA, Australia.
Sam W HendersonAquaporin Physiology and Drug Discovery Program, School of Biomedicine, University of Adelaide, Adelaide, SA, Australia.
Boris MartinacVictor Chang Cardiac Research Institute, Darlinghurst, NSW, Australia.
Osheiza AbdulmalikDivision of Hematology, Children's Hospital of Philadelphia, Philadelphia, PA, United States.
Andrea J YoolAquaporin Physiology and Drug Discovery Program, School of Biomedicine, University of Adelaide, Adelaide, SA, Australia.
University of Adelaide · AUChildren's Hospital of Philadelphia · USSt Vincent's Clinic · AUAustralian National University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In sickle cell disease (SCD), the pathological shift of red blood cells (RBCs) into distorted morphologies under hypoxic conditions follows activation of a cationic leak current (Psickle) and cell dehydration. Prior work showed sickling was reduced by 5-hydroxylmethyl-2-furfural (5-HMF), which stabilized mutant hemoglobin and also blocked the Psickle current in RBCs, though the molecular basis of this 5-HMF-sensitive cation current remained a mystery. Work here is the first to test the hypothesis that Aquaporin-1 (AQP1) cation channels contribute to the monovalent component of Psickle. Human AQP1 channels expressed in

Indexed as

AQP1cyclic GMPerythrocytePiezo1 channelpsickleRBCsickle cell anemia

Identifiers

PMID35111062
PMCPMC8801817
OpenAlexW4206291223

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.