ReviewThe EMBO journal2011
After half a century mitochondrial calcium in- and efflux machineries reveal themselves.
Review in The EMBO journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.
What it found
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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
87 citing papers in PubMed, 176 citations in OpenAlex.
- VPS13A Deficiency Leads to Impaired Lipid Distribution and Alteration of Mitochondrial Calcium Homeostasis in Fibroblasts of VPS13A Disease Patients.Movement disorders : official journal of the Movement Disorder Society · 2026Article
- The role of mitochondria-endoplasmic reticulum crosstalk in colorectal cancer.Genes & diseases · 2026Review
- Mitochondrial dysfunction: the hidden catalyst in chronic kidney disease progression.Renal failure · 2025Review
- The perspective of modern transplant science - transplant arteriosclerosis: inspiration derived from mitochondria associated endoplasmic reticulum membrane dysfunction in arterial diseases.International journal of surgery (London, England) · 2025Review
- Loss of mitochondrial CaCell communication and signaling : CCS · 2024Article
- NCLX controls hepatic mitochondrial CaMolecular metabolism · 2024Article
- Endoplasmic reticulum stress in diseases.MedComm · 2024Review
- Mrs2-mediated mitochondrial magnesium uptake is essential for the regulation of MCU-mediated mitochondrial CaMitochondrion · 2024Article
- Mitochondrial dynamics in health and disease: mechanisms and potential targets.Signal transduction and targeted therapy · 2023Review
- Haploid Parthenogenetic Embryos Exhibit Unique Stress Response to pH, Osmotic and Oxidative Stress.Reproductive sciences (Thousand Oaks, Calif.) · 2023Article
- The multifaceted roles of natural products in mitochondrial dysfunction.Frontiers in pharmacology · 2023Review
- Mitochondrial calcium cycling in neuronal function and neurodegeneration.Frontiers in cell and developmental biology · 2023Review
- Calcium Overload and Mitochondrial Metabolism.Biomolecules · 2022Review
- Stimulation of the mitochondrial calcium uniporter mitigates chronic heart failure-associated ventricular arrhythmia in mice.Heart rhythm · 2022Article
- Mitochondrial CaInternational journal of molecular sciences · 2022Review
- Calcium Signalling in Breast Cancer Associated Bone Pain.International journal of molecular sciences · 2022Review
- Therapeutic Strategies Targeting Mitochondrial Calcium Signaling: A New Hope for Neurological Diseases?Antioxidants (Basel, Switzerland) · 2022Review
- Calcium Ions Signaling: Targets for Attack and Utilization by Viruses.Frontiers in microbiology · 2022Review
- Genome-Wide Identification of Wild Soybean Mitochondrial Calcium Uniporter Family Genes and Their Responses to Cold and Carbonate Alkaline Stresses.Frontiers in plant science · 2022Article
- Mitochondria and Mitochondrial DNA: Key Elements in the Pathogenesis and Exacerbation of the Inflammatory State Caused by COVID-19.Medicina (Kaunas, Lithuania) · 2021Review
27 more citing papers are in PubMed but not listed here.
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 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial Ca(2+) uptake and release play a fundamental role in the control of different physiological processes, such as cytoplasmic Ca(2+) signalling, ATP production and hormone metabolism, while dysregulation of mitochondrial Ca(2+) handling triggers the cascade of events that lead to cell death. The basic mechanisms of mitochondrial Ca(2+) homeostasis have been firmly established for decades, but the molecular identities of the channels and transporters responsible for Ca(2+) uptake and release have remained mysterious until very recently. Here, we briefly review the main findings that have led to our present understanding of mitochondrial Ca(2+) homeostasis and its integration in cell physiology. We will then discuss the recent work that has unravelled the biochemical identity of three key molecules: NCLX, the mitochondrial Na(+)/Ca(2+) antiporter, MCU, the pore-forming subunit of the mitochondrial Ca(2+) uptake channel, and MICU1, one of its regulatory subunits.
Indexed as
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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.