ArticleJournal of molecular and cellular cardiology2013
NCLX: the mitochondrial sodium calcium exchanger.
Article in Journal of molecular and cellular cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 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
84 citing papers in PubMed, 157 citations in OpenAlex.
- Mitochondrial calcium regulates lipid metabolism by modulating tethering of mitochondria to lipid droplets.The EMBO journal · 2026Article
- The two faces of mitochondrial CaJournal of physiology and biochemistry · 2026Review
- Cellular aspects of NaQuantitative plant biology · 2026Review
- Assessment of mitochondrial viability under calcium Stress: Insights for mitochondrial transplantation.Mitochondrion · 2026Article
- Calcium transport systems as virulence determinants: Mechanistic insights into fungal pathogenicity and antifungal resistance.Virulence · 2025Review
- A simulation study on the role of mitochondria-sarcoplasmic reticulum CaThe Journal of physiology · 2025Article
- Review
- Review
- Article
- Calcium signaling in postsynaptic mitochondria: mechanisms, dynamics, and role in ATP production.Frontiers in molecular neuroscience · 2025Review
- Calcium-mediated regulation of mitophagy: implications in neurodegenerative diseases.npj metabolic health and disease · 2025Review
- Loss of mitochondrial CaCell communication and signaling : CCS · 2024Article
- MCU genetically altered mice suggest how mitochondrial CaTrends in endocrinology and metabolism: TEM · 2024Review
- Effects of lithium isotopes on sodium/lithium co-transport and calcium efflux through the sodium/calcium/lithium exchanger in mitochondria.Frontiers in physiology · 2024Article
- Patch-clamp technique to study mitochondrial membrane biophysics.The Journal of general physiology · 2023Article
- Beyond the matrix: structural and physiological advancements in mitochondrial calcium signaling.Biochemical Society transactions · 2023Review
- Mitochondrial responses to intracellular CaJournal of neurophysiology · 2023Article
- Sodium perturbs mitochondrial respiration and induces dysfunctional Tregs.Cell metabolism · 2023Article
- Article
- Insights fromFrontiers in neuroscience · 2023Review
24 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
5 authors at 4 institutions in 2 countries.
Funding
Abstract
The free Ca(2+) concentration within the mitochondrial matrix ([Ca(2+)]m) regulates the rate of ATP production and other [Ca(2+)]m sensitive processes. It is set by the balance between total Ca(2+) influx (through the mitochondrial Ca(2+) uniporter (MCU) and any other influx pathways) and the total Ca(2+) efflux (by the mitochondrial Na(+)/Ca(2+) exchanger and any other efflux pathways). Here we review and analyze the experimental evidence reported over the past 40years which suggest that in the heart and many other mammalian tissues a putative Na(+)/Ca(2+) exchanger is the major pathway for Ca(2+) efflux from the mitochondrial matrix. We discuss those reports with respect to a recent discovery that the protein product of the human FLJ22233 gene mediates such Na(+)/Ca(2+) exchange across the mitochondrial inner membrane. Among its many functional similarities to other Na(+)/Ca(2+) exchanger proteins is a unique feature: it efficiently mediates Li(+)/Ca(2+) exchange (as well as Na(+)/Ca(2+) exchange) and was therefore named NCLX. The discovery of NCLX provides both the identity of a novel protein and new molecular means of studying various unresolved quantitative aspects of mitochondrial Ca(2+) movement out of the matrix. Quantitative and qualitative features of NCLX are discussed as is the controversy regarding the stoichiometry of the NCLX Na(+)/Ca(2+) exchange, the electrogenicity of NCLX, the [Na(+)]i dependency of NCLX and the magnitude of NCLX Ca(2+) efflux. Metabolic features attributable to NCLX and the physiological implication of the Ca(2+) efflux rate via NCLX during systole and diastole are also briefly discussed.
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.