ReviewThe journal of physiological sciences : JPS2015
The destiny of Ca(2+) released by mitochondria.
Review in The journal of physiological sciences : JPS, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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.
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.
Who cites it
38 citing papers in PubMed, 72 citations in OpenAlex.
- A simulation study on the role of mitochondria-sarcoplasmic reticulum CaThe Journal of physiology · 2025Article
- The multifaceted role of mitochondria in autism spectrum disorder.Molecular psychiatry · 2025Review
- Endoplasmic Reticulum and Mitochondrial Calcium Handling Dynamically Shape Slow Afterhyperpolarizations in Vasopressin Magnocellular Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Cell-specific modulation of mitochondrial respiration and metabolism by the pro-apoptotic Bcl-2 family members Bax and Bak.Apoptosis : an international journal on programmed cell death · 2024Article
- Sepsis‑induced cardiac dysfunction and pathogenetic mechanisms (Review).Molecular medicine reports · 2023Review
- Increased retention of functional mitochondria in mature sickle red blood cells is associated with increased sickling tendency, hemolysis and oxidative stress.Haematologica · 2023Article
- Diversity and complexity of cell death: a historical review.Experimental & molecular medicine · 2023Review
- Secretome as neuropathology-targeted intervention of Parkinson's disease.Regenerative therapy · 2022Review
- Spatial and Functional Crosstalk between the Mitochondrial NaInternational journal of molecular sciences · 2022Article
- CaPflugers Archiv : European journal of physiology · 2022Review
- Biochemical properties of HCurrent research in physiology · 2022Article
- Physiological and Pathophysiological Roles of Mitochondrial NaBiomolecules · 2021Review
- A common genetic variant of a mitochondrial RNA processing enzyme predisposes to insulin resistance.Science advances · 2021Article
- Abnormalities of synaptic mitochondria in autism spectrum disorder and related neurodevelopmental disorders.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Regulation of Cell Death by Mitochondrial Transport Systems of Calcium and Bcl-2 Proteins.Membranes · 2020Review
- Regulation of cellular senescence by eukaryotic members of the FAH superfamily - A role in calcium homeostasis?Mechanisms of ageing and development · 2020Review
- Membrane current evoked by mitochondrial NaThe journal of physiological sciences : JPS · 2020Article
- Effects of aging and exercise training on mitochondrial function and apoptosis in the rat heart.Pflugers Archiv : European journal of physiology · 2020Article
- Relationship Between Mitochondrial Structure and Bioenergetics inFrontiers in cell and developmental biology · 2020Article
- Total Matrix CaFrontiers in physiology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial Ca(2+) is known to regulate diverse cellular functions, for example energy production and cell death, by modulating mitochondrial dehydrogenases, inducing production of reactive oxygen species, and opening mitochondrial permeability transition pores. In addition to the action of Ca(2+) within mitochondria, Ca(2+) released from mitochondria is also important in a variety of cellular functions. In the last 5 years, the molecules responsible for mitochondrial Ca(2+) dynamics have been identified: a mitochondrial Ca(2+) uniporter (MCU), a mitochondrial Na(+)-Ca(2+) exchanger (NCLX), and a candidate for a mitochondrial H(+)-Ca(2+) exchanger (Letm1). In this review, we focus on the mitochondrial Ca(2+) release system, and discuss its physiological and pathophysiological significance. Accumulating evidence suggests that the mitochondrial Ca(2+) release system is not only crucial in maintaining mitochondrial Ca(2+) homeostasis but also participates in the Ca(2+) crosstalk between mitochondria and the plasma membrane and between mitochondria and the endoplasmic/sarcoplasmic reticulum.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.