Evidence map›Paper›PMID 27458051›Full record

ArticleScientific reports2016

Mitochondrial Mg(2+) homeostasis decides cellular energy metabolism and vulnerability to stress.

Ryu Yamanaka, Sho Tabata, Yutaka Shindo, Kohji Hotta, Koji Suzuki, Tomoyoshi Soga, Kotaro Oka

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 3% 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

86 citing papers in PubMed, 1 synthesis or guideline pooled it, 147 citations in OpenAlex.

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  17. Structure and function of the human mitochondrial MRS2 channel.Nature structural & molecular biology · 2025
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26 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Ryu YamanakaCenter for Biosciences and Informatics, School of Fundamental Science and Technology Graduate School of Science and Technology, Keio University, Yokohama, 223-8522, Kanagawa, Japan.
Sho TabataInstitute for Advanced Biosciences, Keio University, Kakuganji, Tsuruoka, Yamagata, 997-0052, Japan.
Yutaka ShindoCenter for Biosciences and Informatics, School of Fundamental Science and Technology Graduate School of Science and Technology, Keio University, Yokohama, 223-8522, Kanagawa, Japan.
Kohji HottaCenter for Biosciences and Informatics, School of Fundamental Science and Technology Graduate School of Science and Technology, Keio University, Yokohama, 223-8522, Kanagawa, Japan.
Koji SuzukiCenter for Science and Technology for Designing Functions, School of Integrated Design Engineering, Graduate School of Science and Technology, Keio University, Yokohama, Kanagawa, 223-8522, Japan.
Tomoyoshi SogaInstitute for Advanced Biosciences, Keio University, Kakuganji, Tsuruoka, Yamagata, 997-0052, Japan.
Kotaro OkaCenter for Biosciences and Informatics, School of Fundamental Science and Technology Graduate School of Science and Technology, Keio University, Yokohama, 223-8522, Kanagawa, Japan.
Keio University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular energy production processes are composed of many Mg(2+) dependent enzymatic reactions. In fact, dysregulation of Mg(2+) homeostasis is involved in various cellular malfunctions and diseases. Recently, mitochondria, energy-producing organelles, have been known as major intracellular Mg(2+) stores. Several biological stimuli alter mitochondrial Mg(2+) concentration by intracellular redistribution. However, in living cells, whether mitochondrial Mg(2+) alteration affect cellular energy metabolism remains unclear. Mg(2+) transporter of mitochondrial inner membrane MRS2 is an essential component of mitochondrial Mg(2+) uptake system. Here, we comprehensively analyzed intracellular Mg(2+) levels and energy metabolism in Mrs2 knockdown (KD) cells using fluorescence imaging and metabolome analysis. Dysregulation of mitochondrial Mg(2+) homeostasis disrupted ATP production via shift of mitochondrial energy metabolism and morphology. Moreover, Mrs2 KD sensitized cellular tolerance against cellular stress. These results indicate regulation of mitochondrial Mg(2+) via MRS2 critically decides cellular energy status and cell vulnerability via regulation of mitochondrial Mg(2+) level in response to physiological stimuli.

Indexed as

Biological TransportCation Transport ProteinsCell Line, TumorCell Physiological PhenomenaEnergy MetabolismHeLa CellsHomeostasisHumansMagnesiumMembrane Potential, MitochondrialMitochondriaMitochondrial ProteinsRNA InterferenceRNA, Small InterferingStress, PhysiologicalCation Transport ProteinsMagnesiumMitochondrial ProteinsMRS2 protein, humanRNA, Small Interfering

Identifiers

PMID27458051
PMCPMC4960558
OpenAlexW2502719111

What OpenQuestion holds

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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.