ArticleThe Journal of general physiology2012
Dynamics of matrix-free Ca2+ in cardiac mitochondria: two components of Ca2+ uptake and role of phosphate buffering.
Article in The Journal of general physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 79 citations in OpenAlex.
- Mechanistic basis of EMRE's essential role in the regulation of mitochondrial calcium uniporter complex.bioRxiv : the preprint server for biology · 2026Article
- Mitochondrial CaJournal of cellular physiology · 2025Review
- How does mitochondrial Ca2+ change during ischemia and reperfusion? Implications for activation of the permeability transition pore.The Journal of general physiology · 2025Review
- Cyclophilin D plays a critical role in the survival of senescent cells.The EMBO journal · 2024Article
- Mitochondrial Calcium Regulation of Cardiac Metabolism in Health and Disease.Physiology (Bethesda, Md.) · 2024Review
- Metabolically regulated spiking could serve neuronal energy homeostasis and protect from reactive oxygen species.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Physiology of intracellular calcium buffering.Physiological reviews · 2023Review
- Increased mitochondrial free CaCell reports · 2023Article
- Post-translational modifications and protein quality control of mitochondrial channels and transporters.Frontiers in cell and developmental biology · 2023Review
- Calcium Overload and Mitochondrial Metabolism.Biomolecules · 2022Review
- SR-Mitochondria Crosstalk Shapes Ca Signalling to Impact Pathophenotype in Disease Models Marked by Dysregulated Intracellular Ca Release.Cardiovascular research · 2022Article
- A controversial issue: Can mitochondria modulate cytosolic calcium and contraction of skeletal muscle fibers?The Journal of general physiology · 2022Review
- Mitochondrial calcium exchange in physiology and disease.Physiological reviews · 2022Review
- Oxidative Stress Related to Plasmalemmal and Mitochondrial Phosphate Transporters in Vascular Calcification.Antioxidants (Basel, Switzerland) · 2022Review
- Differences in molecular phenotype in mouse and human hypertrophic cardiomyopathy.Scientific reports · 2021Article
- Mitochondrial CaJournal of molecular and cellular cardiology · 2021Review
- The debate continues - What is the role of MCU and mitochondrial calcium uptake in the heart?Journal of molecular and cellular cardiology · 2020Review
- Why don't mice lacking the mitochondrial CaThe Journal of physiology · 2020Review
- Calcium Signaling in Cardiomyocyte Function.Cold Spring Harbor perspectives in biology · 2020Review
- Global knockout of ROMK potassium channel worsens cardiac ischemia-reperfusion injury but cardiomyocyte-specific knockout does not: Implications for the identity of mitoKATP.Journal of molecular and cellular cardiology · 2020Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mitochondrial Ca(2+) uptake is thought to provide an important signal to increase energy production to meet demand but, in excess, can also trigger cell death. The mechanisms defining the relationship between total Ca(2+) uptake, changes in mitochondrial matrix free Ca(2+), and the activation of the mitochondrial permeability transition pore (PTP) are not well understood. We quantitatively measure changes in [Ca(2+)](out) and [Ca(2+)](mito) during Ca(2+) uptake in isolated cardiac mitochondria and identify two components of Ca(2+) influx. [Ca(2+)](mito) recordings revealed that the first, MCU(mode1), required at least 1 µM Ru360 to be completely inhibited, and responded to small Ca(2+) additions in the range of 0.1 to 2 µM with rapid and large changes in [Ca(2+)](mito). The second component, MCU(mode2), was blocked by 100 nM Ru360 and was responsible for the bulk of total Ca(2+) uptake for large Ca(2+) additions in the range of 2 to 10 µM; however, it had little effect on steady-state [Ca(2+)](mito). MCU(mode1) mediates changes in [Ca(2+)](mito) of 10s of μM, even in the presence of 100 nM Ru360, indicating that there is a finite degree of Ca(2+) buffering in the matrix associated with this pathway. In contrast, the much higher Ca(2+) loads evoked by MCU(mode2) activate a secondary dynamic Ca(2+) buffering system consistent with calcium-phosphate complex formation. Increasing P(i) potentiated [Ca(2+)](mito) increases via MCU(mode1) but suppressed [Ca(2+)](mito) changes via MCU(mode2). The results suggest that the role of MCU(mode1) might be to modulate oxidative phosphorylation in response to intracellular Ca(2+) signaling, whereas MCU(mode2) and the dynamic high-capacity Ca(2+) buffering system constitute a Ca(2+) sink function. Interestingly, the trigger for PTP activation is unlikely to be [Ca(2+)](mito) itself but rather a downstream byproduct of total mitochondrial Ca(2+) loading.
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Registered trials
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