Evidence map›Paper›PMID 35624667›Full record

ReviewAntioxidants (Basel, Switzerland)2022

Mitochondrial Calcium: Effects of Its Imbalance in Disease.

Deyamira Matuz-Mares, Martin González-Andrade, Minerva Georgina Araiza-Villanueva, María Magdalena Vilchis-Landeros, Héctor Vázquez-Meza

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed
17.5field-weighted citation impact, top 1% 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

140 citing papers in PubMed, 224 citations in OpenAlex.

  1. Review
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  3. The Effects of Disrupting CaMarine biotechnology (New York, N.Y.) · 2026
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  15. Aloin attenuates NMDA receptor by modulating calcium response on substantia gelatinosa neurons of the trigeminal subnucleus caudalis in mice.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
    Article
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  18. Review
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  20. Article

80 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

5 authors at 2 institutions in 2 countries.

Deyamira Matuz-MaresDepartamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México, Avenida Universidad 3000, Cd. Universitaria, Coyoacán, Ciudad de México 04510, Mexico.
Martin González-AndradeDepartamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México, Avenida Universidad 3000, Cd. Universitaria, Coyoacán, Ciudad de México 04510, Mexico.ORCID 0000-0002-8910-3035
Minerva Georgina Araiza-VillanuevaInstitute of Microbiology, Heinrich Heine University Düsseldorf, 40204 Düsseldorf, Germany.
María Magdalena Vilchis-LanderosDepartamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México, Avenida Universidad 3000, Cd. Universitaria, Coyoacán, Ciudad de México 04510, Mexico.
Héctor Vázquez-MezaDepartamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México, Avenida Universidad 3000, Cd. Universitaria, Coyoacán, Ciudad de México 04510, Mexico.ORCID 0000-0002-8312-3115
Universidad Nacional Autónoma de México · MXHeinrich Heine University Düsseldorf · DE

Funding

UNAM-PAPIIT IN203222UNAM-PAPIIT IN218821
6 · The paper itself

Abstract

Calcium is used in many cellular processes and is maintained within the cell as free calcium at low concentrations (approximately 100 nM), compared with extracellular (millimolar) concentrations, to avoid adverse effects such as phosphate precipitation. For this reason, cells have adapted buffering strategies by compartmentalizing calcium into mitochondria and the endoplasmic reticulum (ER). In mitochondria, the calcium concentration is in the millimolar range, as it is in the ER. Mitochondria actively contribute to buffering cellular calcium, but if matrix calcium increases beyond physiological demands, it can promote the opening of the mitochondrial permeability transition pore (mPTP) and, consequently, trigger apoptotic or necrotic cell death. The pathophysiological implications of mPTP opening in ischemia-reperfusion, liver, muscle, and lysosomal storage diseases, as well as those affecting the central nervous system, for example, Parkinson's disease (PD), Alzheimer's disease (AD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS) have been reported. In this review, we present an updated overview of the main cellular mechanisms of mitochondrial calcium regulation. We specially focus on neurodegenerative diseases related to imbalances in calcium homeostasis and summarize some proposed therapies studied to attenuate these diseases.

Indexed as

calciumdiseasemitochondrianeurodegenerative

Identifiers

PMID35624667
PMCPMC9138001
OpenAlexW4224267474

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.