ReviewCell calcium2012
The permeability transition pore as a Ca(2+) release channel: new answers to an old question.
Review in Cell calcium, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 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.
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Who cites it
91 citing papers in PubMed.
- ATP synthase subunits e and g are essential for CaCell death and differentiation · 2026Article
- Article
- Aberrant myocardial calcium cycling: pathogenic mechanisms and targeted therapeutics for heart failure.Frontiers in cardiovascular medicine · 2026Review
- A Mitochondrial Basis for Heart Failure Progression.Cardiovascular drugs and therapy · 2024Review
- Cyclophilin D plays a critical role in the survival of senescent cells.The EMBO journal · 2024Article
- Extracellular freezing induces a permeability transition in the inner membrane of muscle mitochondria of freeze-sensitive but not freeze-tolerantFrontiers in physiology · 2024Article
- Mitochondrial dysfunction in pancreatic acinar cells: mechanisms and therapeutic strategies in acute pancreatitis.Frontiers in immunology · 2024Review
- Mechanism and treatment of intracerebral hemorrhage focus on mitochondrial permeability transition pore.Frontiers in molecular neuroscience · 2024Review
- Signaling Roleplay between Ion Channels during Mammalian Sperm Capacitation.Biomedicines · 2023Review
- Identity, structure, and function of the mitochondrial permeability transition pore: controversies, consensus, recent advances, and future directions.Cell death and differentiation · 2023Review
- Role of the Mitochondrial Permeability Transition in Bone Metabolism and Aging.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023Article
- Mitochondrial Dysfunction in Intensive Care Unit-Acquired Weakness and Critical Illness Myopathy: A Narrative Review.International journal of molecular sciences · 2023Review
- Review
- Defective excitation-contraction coupling and mitochondrial respiration precede mitochondrial CaNature communications · 2023Article
- Long-term potentiation and spatial memory training stimulate the hippocampal expression of RyR2 calcium release channels.Frontiers in cellular neuroscience · 2023Article
- Mitochondrial Permeability Transition in Stem Cells, Development, and Disease.Advances in experimental medicine and biology · 2023Review
- Non-conventional mitochondrial permeability transition: Its regulation by mitochondrial dynamics.Biochimica et biophysica acta. Bioenergetics · 2023Article
- SR-Mitochondria Crosstalk Shapes Ca Signalling to Impact Pathophenotype in Disease Models Marked by Dysregulated Intracellular Ca Release.Cardiovascular research · 2022Article
- Remodeling of Liver and Plasma Lipidomes in Mice Lacking Cyclophilin D.International journal of molecular sciences · 2022Article
- Article
31 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
2 authors.
Funding
Abstract
Mitochondria possess a sophisticated array of Ca(2+) transport systems reflecting their key role in physiological Ca(2+) homeostasis. With the exception of most yeast strains, energized organelles are endowed with a very fast and efficient mechanism for Ca(2+) uptake, the ruthenium red (RR)-sensitive mitochondrial Ca(2+) uniporter (MCU); and one main mechanism for Ca(2+) release, the RR-insensitive 3Na(+)-Ca(2+) antiporter. An additional mechanism for Ca(2+) release is provided by a Na(+) and RR-insensitive release mechanism, the putative 3H(+)-Ca(2+) antiporter. A potential kinetic imbalance is present, however, because the V(max) of the MCU is of the order of 1400nmol Ca(2+)mg(-1) proteinmin(-1) while the combined V(max) of the efflux pathways is about 20nmol Ca(2+)mg(-1) proteinmin(-1). This arrangement exposes mitochondria to the hazards of Ca(2+) overload when the rate of Ca(2+) uptake exceeds that of the combined efflux pathways, e.g. for sharp increases of cytosolic [Ca(2+)]. In this short review we discuss the hypothesis that transient opening of the Ca(2+)-dependent permeability transition pore may provide mitocondria with a fast Ca(2+) release channel preventing Ca(2+) overload. We also address the relevance of a mitochondrial Ca(2+) release channel recently discovered in Drosophila melanogaster, which possesses intermediate features between the permeability transition pore of yeast and mammals.
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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.