ReviewPflugers Archiv : European journal of physiology2007
Mitochondria and Ca(2+) signaling: old guests, new functions.
Review in Pflugers Archiv : European journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 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
73 citing papers in PubMed, 157 citations in OpenAlex.
- Advances in understanding the role of mitochondria in renal ischemia-reperfusion injury.Clinical and experimental nephrology · 2025Review
- Review
- Mitochondrial-targeted therapies in traumatic brain injury: From bench to bedside.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Calcium signaling in postsynaptic mitochondria: mechanisms, dynamics, and role in ATP production.Frontiers in molecular neuroscience · 2025Review
- Mitochondrial metabolism and targeted treatment strategies in ischemic-induced acute kidney injury.Cell death discovery · 2024Review
- Alzheimer's Disease Puzzle: Delving into Pathogenesis Hypotheses.Aging and disease · 2024Review
- Review
- The mitochondrial CaScientific reports · 2022Article
- Structural characterization of the mitochondrial CaiScience · 2021Review
- Restriction of an intron size en route to endothermy.Nucleic acids research · 2021Article
- A method for assessing tissue respiration in anatomically defined brain regions.Scientific reports · 2020Article
- Live-Cell Imaging of Physiologically Relevant Metal Ions Using Genetically Encoded FRET-Based Probes.Cells · 2019Review
- Paraneoplastic cerebellar degeneration: Yo antibody alters mitochondrial calcium buffering capacity.Neuropathology and applied neurobiology · 2019Article
- Real-Time Imaging of Mitochondrial ATP Dynamics Reveals the Metabolic Setting of Single Cells.Cell reports · 2018Article
- Alteration in nerves and neurotransmitter stimulation of lacrimal gland secretion in the TSP-1Mucosal immunology · 2018Article
- An adverse outcome pathway for parkinsonian motor deficits associated with mitochondrial complex I inhibition.Archives of toxicology · 2018Review
- Virtual Cell Based Assay simulations of intra-mitochondrial concentrations in hepatocytes and cardiomyocytes.Toxicology in vitro : an international journal published in association with BIBRA · 2017Article
- Nuclear but not mitochondrial-encoded oxidative phosphorylation genes are altered in aging, mild cognitive impairment, and Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2017Article
- The Close Interconnection between Mitochondrial Dynamics and Mitophagy in Cancer.Frontiers in oncology · 2017Review
- Intact mitochondrial CaFree radical biology & medicine · 2017Article
13 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
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Mitochondria are ancient endosymbiotic guests that joined the cells in the evolution of complex life. While the unique ability of mitochondria to produce adenosine triphosphate (ATP) and their contribution to cellular nutrition metabolism received condign attention, our understanding of the organelle's contribution to Ca(2+) homeostasis was restricted to serve as passive Ca(2+) sinks that accumulate Ca(2+) along the organelle's negative membrane potential. This paradigm has changed radically. Nowadays, mitochondria are known to respond to environmental Ca(2+) and to contribute actively to the regulation of spatial and temporal patterns of intracellular Ca(2+) signaling. Accordingly, mitochondria contribute to many signal transduction pathways and are actively involved in the maintenance of capacitative Ca(2+) entry, the accomplishment of Ca(2+) refilling of the endoplasmic reticulum and Ca(2+)-dependent protein folding. Mitochondrial Ca(2+) homeostasis is complex and regulated by numerous, so far, genetically unidentified Ca(2+) channels, pumps and exchangers that concertedly accomplish the organelle's Ca(2+) demand. Notably, mitochondrial Ca(2+) homeostasis and functions are crucially influenced by the organelle's structural organization and motility that, in turn, is controlled by matrix/cytosolic Ca(2+). This review intends to provide a condensed overview on the molecular mechanisms of mitochondrial Ca(2+) homeostasis (uptake, buffering and storage, extrusion), its modulation by other ions, kinases and small molecules, and its contribution to cellular processes as fundamental basis for the organelle's contribution to signaling pathways. Hence, emphasis is given to the structure-to-function and mobility-to-function relationship of the mitochondria and, thereby, bridging our most recent knowledge on mitochondria with the best-established mitochondrial function: metabolism and ATP production.
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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.