ArticleNeuroscience letters2014
Molecular and functional identification of a mitochondrial ryanodine receptor in neurons.
Article in Neuroscience letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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.
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Who cites it
32 citing papers in PubMed, 51 citations in OpenAlex.
- Type-1 Ryanodine Receptor Plays an Important Role in Cardiac Hypertrophy and Heart Failure by Increasing Type-2 Ryanodine Receptor-Mediated Calcium Release.International journal of molecular sciences · 2026Article
- Lipid Metabolism in Relation to Calcium Homeostasis.Advances in experimental medicine and biology · 2026Review
- Investigating the neuroprotective effect of heparin in improving mitochondrial function in rats with cardiac arrest cardiopulmonary resuscitation based on transcriptome sequencing.Frontiers in medicine · 2025Article
- Calcium-mediated regulation of mitophagy: implications in neurodegenerative diseases.npj metabolic health and disease · 2025Review
- Dialogue between mitochondria and endoplasmic reticulum-potential therapeutic targets for age-related cardiovascular diseases.Frontiers in pharmacology · 2024Review
- Mitochondrial CaCommunications biology · 2022Article
- A CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Mitochondrial calcium exchange in physiology and disease.Physiological reviews · 2022Review
- Methods of Measuring Mitochondrial Potassium Channels: A Critical Assessment.International journal of molecular sciences · 2022Review
- Resveratrol Treatment in HumanBiomolecules · 2021Article
- Dual-process brain mitochondria isolation preserves function and clarifies protein composition.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Abnormalities of synaptic mitochondria in autism spectrum disorder and related neurodevelopmental disorders.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Endoplasmic Reticulum-Mitochondria Contacts: A Potential Therapy Target for Cardiovascular Remodeling-Associated Diseases.Frontiers in cell and developmental biology · 2021Review
- Endoplasmic Reticulum-Based Calcium Dysfunctions in Synucleinopathies.Frontiers in neurology · 2021Review
- Endoplasmic reticulum stress serves an important role in cardiac ischemia/reperfusion injury (Review).Experimental and therapeutic medicine · 2020Review
- Mitochondrial Calcium Uniporter (MCU) deficiency reveals an alternate path for CaScientific reports · 2020Article
- The pore-forming subunit MCU of the mitochondrial CaDiabetologia · 2020Article
- Cytoplasmic and Mitochondrial Calcium Signaling: A Two-Way Relationship.Cold Spring Harbor perspectives in biology · 2019Review
- Role of mitochondrial calcium uniporter-mediated CaJournal of cellular and molecular medicine · 2019Article
- Dantrolene : From Malignant Hyperthermia to Alzheimer's Disease.CNS & neurological disorders drug targets · 2019Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Mitochondrial Ca(2+) controls numerous cell functions, such as energy metabolism, reactive oxygen species generation, spatiotemporal dynamics of Ca(2+) signaling, cell growth and death in various cell types including neurons. Mitochondrial Ca(2+) accumulation is mainly mediated by the mitochondrial Ca(2+) uniporter (MCU), but recent reports also indicate that mitochondrial Ca(2+)-influx mechanisms are regulated not only by MCU, but also by multiple channels/transporters. We previously reported that ryanodine receptor (RyR), which is a one of the main Ca(2+)-release channels at endoplasmic/sarcoplasmic reticulum (SR/ER) in excitable cells, is expressed at the mitochondrial inner membrane (IMM) and serves as a part of the Ca(2+) uptake mechanism in cardiomyocytes. Although RyR is also expressed in neuronal cells and works as a Ca(2+)-release channel at ER, it has not been well investigated whether neuronal mitochondria possess RyR and, if so, whether this mitochondrial RyR has physiological functions in neuronal cells. Here we show that neuronal mitochondria express RyR at IMM and accumulate Ca(2+) through this channel in response to cytosolic Ca(2+) elevation, which is similar to what we observed in another excitable cell-type, cardiomyocytes. In addition, the RyR blockers dantrolene or ryanodine significantly inhibits mitochondrial Ca(2+) uptake in permeabilized striatal neurons. Taken together, we identify RyR as an additional mitochondrial Ca(2+) uptake mechanism in response to the elevation of [Ca(2+)]c in neurons, suggesting that this channel may play a critical role in mitochondrial Ca(2+)-mediated functions such as energy metabolism.
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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.