Evidence map›Paper›PMID 38413581›Full record

ArticleNature communications2024

Bicarbonate signalling via G protein-coupled receptor regulates ischaemia-reperfusion injury.

Airi Jo-Watanabe, Toshiki Inaba, Takahiro Osada, Ryota Hashimoto, Tomohiro Nishizawa, Toshiaki Okuno, Sayoko Ihara, Kazushige Touhara, Nobutaka Hattori, Masatsugu Oh-Hora and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
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  10. Sodium Bicarbonate Decreases Alcohol Consumption in Mice.International journal of molecular sciences · 2024
    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

12 authors at 5 institutions in 1 country.

Airi Jo-WatanabeDepartment of Biochemistry, Juntendo University Graduate School of Medicine, Tokyo, 113-8421, Japan. awatanabe-tky@umin.ac.jp.ORCID 0000-0003-0899-9915
Toshiki InabaDepartment of Neurology, Juntendo University School of Medicine, Tokyo, 113-8421, Japan.
Takahiro OsadaDepartment of Neurophysiology, Juntendo University School of Medicine, Tokyo, 113-8421, Japan.ORCID 0000-0002-3743-3200
Ryota HashimotoLaboratory of Cell Biology, Biomedical Research Core Facilities, Juntendo University Graduate School of Medicine, Tokyo, 113-8421, Japan.ORCID 0000-0003-0983-6704
Tomohiro NishizawaGraduate School of Medical Life Science, Yokohama City University, Kanagawa, 230-0045, Japan.ORCID 0000-0001-7463-8398
Toshiaki OkunoDepartment of Biochemistry, Juntendo University Graduate School of Medicine, Tokyo, 113-8421, Japan.
Sayoko IharaDepartment of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, 113-8657, Japan.
Kazushige TouharaDepartment of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, 113-8657, Japan.
Nobutaka HattoriDepartment of Neurology, Juntendo University School of Medicine, Tokyo, 113-8421, Japan.ORCID 0000-0002-2034-2556
Masatsugu Oh-HoraDepartment of Biochemistry, Juntendo University Graduate School of Medicine, Tokyo, 113-8421, Japan.ORCID 0000-0002-2812-6559
Osamu NurekiDepartment of Biological Sciences, Graduate School of Science, The University of Tokyo, Tokyo, 113-0033, Japan.ORCID 0000-0003-1813-7008
Takehiko YokomizoDepartment of Biochemistry, Juntendo University Graduate School of Medicine, Tokyo, 113-8421, Japan. yokomizo-tky@umin.ac.jp.ORCID 0000-0002-5219-1553
Juntendo University · JPThe University of Tokyo · JPJapan Agency for Medical Research and Development · JPRIKEN Center for Brain Science · JPYokohama City University · JP

Funding

Japan Agency for Medical Research and Development (AMED) JP20gm6210026MEXT | Japan Society for the Promotion of Science (JSPS) JP18K15051 and 20K16148
6 · The paper itself

Abstract

Homoeostatic regulation of the acid-base balance is essential for cellular functional integrity. However, little is known about the molecular mechanism through which the acid-base balance regulates cellular responses. Here, we report that bicarbonate ions activate a G protein-coupled receptor (GPCR), i.e., GPR30, which leads to G

Indexed as

Brain IschemiaReperfusion InjuryStrokeAnimalsBicarbonatesCalciumMaleMiceReceptors, EstrogenReceptors, G-Protein-CoupledBicarbonatesCalciumReceptors, EstrogenReceptors, G-Protein-Coupled

Identifiers

PMID38413581
PMCPMC10899177
OpenAlexW4392198390

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.