Evidence map›Paper›PMID 33808082›Full record

ArticleInternational journal of molecular sciences2021

Id2 Represses Aldosterone-Stimulated Cardiac T-Type Calcium Channels Expression.

Jumpei Ito, Tomomi Minemura, Sébastien Wälchli, Tomoaki Niimi, Yoshitaka Fujihara, Shun'ichi Kuroda, Koichi Takimoto, Andrés D Maturana

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

8 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Genetic loci responsible for atrioventricular block in children.Frontiers in cell and developmental biology · 2026
    Review
  3. Article
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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

8 authors at 4 institutions in 2 countries.

Jumpei ItoLaboratory of Animal Cell Physiology, Graduate School of Bioagricultural Sciences, Nagoya University, Aichi 464-8601, Japan.ORCID 0000-0001-5149-9962
Tomomi MinemuraLaboratory of Animal Cell Physiology, Graduate School of Bioagricultural Sciences, Nagoya University, Aichi 464-8601, Japan.
Sébastien WälchliTranslational Research Unit, Section for Cellular Therapy, Oslo University Hospital, 0379 Oslo, Norway.ORCID 0000-0001-5869-1746
Tomoaki NiimiLaboratory of Animal Cell Physiology, Graduate School of Bioagricultural Sciences, Nagoya University, Aichi 464-8601, Japan.
Yoshitaka FujiharaDepartment of Experimental Genome Research, Research Institute for Microbial Diseases, Osaka 565-0871, Japan.ORCID 0000-0001-8332-3507
Shun'ichi KurodaInstitute for Scientific and Industrial Researches, Osaka University, Osaka 567-0047, Japan.ORCID 0000-0002-5432-7274
Koichi TakimotoDepartment of Bioengineering, Nagaoka University of Technology, Nagaoka 940-2188, Japan.
Andrés D MaturanaLaboratory of Animal Cell Physiology, Graduate School of Bioagricultural Sciences, Nagoya University, Aichi 464-8601, Japan.
Nagoya University · JPNagaoka University of Technology · JPOsaka Research Institute of Industrial Science and Technology · JPOslo University Hospital · NO

Funding

Japan Society for the Promotion of Science 24570150
6 · The paper itself

Abstract

Aldosterone excess is a cardiovascular risk factor. Aldosterone can directly stimulate an electrical remodeling of cardiomyocytes leading to cardiac arrhythmia and hypertrophy. L-type and T-type voltage-gated calcium (Ca

Indexed as

AldosteroneAnimalsCalcium Channels, T-TypeCells, CulturedGene Expression RegulationHeartInhibitor of Differentiation Protein 2Mice, TransgenicMyocytes, CardiacAldosteroneCacna1g protein, ratCalcium Channels, T-TypeId2 protein, ratInhibitor of Differentiation Protein 2aldosteronecardiomyocytesT-type calcium channels (List three to ten pertinent keywords specific to the article yet reasonably common within the subject discipline.)

Identifiers

PMID33808082
PMCPMC8037527
OpenAlexW3141374846

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.