ReviewThe FEBS journal2010
The molecular identity of the mitochondrial Ca2+ sequestration system.
Review in The FEBS journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 67 citations in OpenAlex.
- Cyclophilin D reduces Ca2+ sequestration by complement 1q binding protein.The Biochemical journal · 2025Article
- Differential CaFrontiers in synaptic neuroscience · 2025Article
- Endogenous complement 1q binding protein (C1qbp) regulates mitochondrial permeability transition and post-myocardial infarction remodeling and dysfunction.Journal of molecular and cellular cardiology · 2024Article
- Neuroprotective effects of dantrolene in neurodegenerative disease: Role of inhibition of pathological inflammation.Journal of anesthesia and translational medicine · 2024Article
- Mitochondrial morphology in the mouse adrenal cortex: Influence of chronic psychosocial stress.Psychoneuroendocrinology · 2024Article
- Regulation of cellular senescence by eukaryotic members of the FAH superfamily - A role in calcium homeostasis?Mechanisms of ageing and development · 2020Review
- The Emerging Role ofFrontiers in neurology · 2020Review
- Total Matrix CaFrontiers in physiology · 2020Article
- Article
- Emerging molecular therapeutic targets for spinal cord injury.Expert opinion on therapeutic targets · 2019Review
- Effects of Phenelzine Administration on Mitochondrial Function, Calcium Handling, and Cytoskeletal Degradation after Experimental Traumatic Brain Injury.Journal of neurotrauma · 2019Article
- Arginase II Contributes to the CaJournal of the American Heart Association · 2018Article
- In vitro and in vivo studies of the ALS-FTLD protein CHCHD10 reveal novel mitochondrial topology and protein interactions.Human molecular genetics · 2018Article
- Mitochondrial-Based Therapeutics for the Treatment of Spinal Cord Injury: Mitochondrial Biogenesis as a Potential Pharmacological Target.The Journal of pharmacology and experimental therapeutics · 2017Review
- IDH3 mediates apoptosis of alveolar epithelial cells type 2 due to mitochondrial CaCell death & disease · 2017Article
- Mitochondrial permeability transition in cardiac ischemia-reperfusion: whether cyclophilin D is a viable target for cardioprotection?Cellular and molecular life sciences : CMLS · 2017Review
- Mutant TDP-43 does not impair mitochondrial bioenergetics in vitro and in vivo.Molecular neurodegeneration · 2017Article
- TrpA1 activation in peripheral sensory neurons underlies the ionic basis of pain hypersensitivity in response to vinca alkaloids.PloS one · 2017Article
- Mitochondrial Ca(2+) uptake in skeletal muscle health and disease.Science China. Life sciences · 2016Review
- In vitro analyses of mitochondrial ATP/phosphate carriers from Arabidopsis thaliana revealed unexpected Ca(2+)-effects.BMC plant biology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
There is ample evidence to suggest that a dramatic decrease in mitochondrial Ca(2+) retention may contribute to the cell death associated with stroke, excitotoxicity, ischemia and reperfusion, and neurodegenerative diseases. Mitochondria from all studied tissues can accumulate and store Ca(2+) , but the maximum Ca(2+) storage capacity varies widely and exhibits striking tissue specificity. There is currently no explanation for this fact. Precipitation of Ca(2+) and phosphate in the mitochondrial matrix has been suggested to be the major form of storage of accumulated Ca(2+) in mitochondria. How this precipitate is formed is not known. The molecular identity of almost all proteins involved in Ca(2+) transport, storage and formation of the permeability transition pore is also unknown. This review summarizes studies aimed at identifying these proteins, and describes the properties of a known mitochondrial protein that may be involved in Ca(2+) transport and the structure of the permeability transition pore.
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.