Evidence mapPaperPMID 42334704Full record

ReviewJournal of physiology and biochemistry2026

The two faces of mitochondrial Ca

Mikhail V Dubinin, Konstantin N Belosludtsev

Abstract readReview
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In one paragraph

Review in Journal of physiology and biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

2 authors.

Mikhail V DubininMari State University, Pl. Lenina 1, Yoshkar-Ola, 424001, Russia. dubinin1989@gmail.com.ORCID http://orcid.org/0000-0002-7453-3390
Konstantin N BelosludtsevInstitute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Institutskaya 3, Pushchino, 142290, Russia.ORCID http://orcid.org/0000-0001-5392-7035

Funding

Russian Science Foundation 25-65-00005
6 · The paper itself

Abstract

Mitochondrial Ca²⁺ dysregulation is a central pathogenic event in skeletal muscle disorders, yet the dichotomy between overload and deficiency is often overlooked. This review summarizes mechanisms governing mitochondrial Ca²⁺ transport and sarcoplasmic reticulum-mitochondria communication. We examine prerequisites of Ca²⁺ overload, including RyR1/SERCA dysfunction and mitochondrial calcium uniporter (MCU) complex remodeling, leading to suppressed ATP synthesis, reactive oxygen species overproduction, and necrosis. Conversely, we address mitochondrial Ca²⁺ deficiency in aging, sarcopenia, and diabetes, resulting from altered MCU stoichiometry and reduced organelle tethering, causing metabolic inflexibility and impaired antioxidant defense. Additionally, therapeutic strategies limiting Ca²⁺ overload and prospects of pharmacological MCU activation to enhance bioenergetics in sarcopenia are discussed.

Indexed as

CalciumCalcium SignalingMitochondria, MuscleMuscle, SkeletalSarcopeniaAgingAnimalsCalcium ChannelsEnergy MetabolismHumansReactive Oxygen SpeciesRyanodine Receptor Calcium Release ChannelSarcoplasmic ReticulumSarcoplasmic Reticulum Calcium-Transporting ATPasesCalciumCalcium Channelsmitochondrial calcium uniporterReactive Oxygen SpeciesRyanodine Receptor Calcium Release ChannelSarcoplasmic Reticulum Calcium-Transporting ATPasesCalcium signalingMCU complexMitochondrial Ca²⁺ deficiencyMitochondrial Ca²⁺ overloadSarcoplasmic reticulum-mitochondria couplingSkeletal muscle

Identifiers

What Socratic holds

Textmetadata
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 Socratic graph.