ReviewCell calcium2012
Mitochondrial Ca(2+) and apoptosis.
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 235 papers, 2 of them syntheses that pooled it.
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
235 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Mitochondrial quality control in neurodegenerative diseases: from molecular mechanisms to natural product therapies.Frontiers in physiology · 2025Pooled it
- Neurotoxic Effects of Neonicotinoids on Mammals: What Is There beyond the Activation of Nicotinic Acetylcholine Receptors?-A Systematic Review.International journal of molecular sciences · 2021Pooled it
- CerS2-mediated lipotoxicity and calcium signaling: a novel sequential mechanism of apoptosis in cancer.The Biochemical journal · 2026Review
- ER proteostasis meets mitochondrial function: contact sites as hubs of communication and therapeutic targets.The FEBS journal · 2026Review
- Heavy metal toxicity as a driver of endoplasmic reticulum stress and dysfunction.The FEBS journal · 2026Review
- Mitochondria‑endoplasmic reticulum contact site nexus: Molecular integration, disease pathogenesis and therapeutic opportunities (Review).International journal of molecular medicine · 2026Review
- Pharmacologic Activation of TRPA1 Induces Multi-Target Anticancer Responses via Apoptotic and Mitochondrial Pathways.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Mitochondrial calcium regulates lipid metabolism by modulating tethering of mitochondria to lipid droplets.The EMBO journal · 2026Article
- Skin capillary endothelial cells form a network of spatiotemporally conserved CaProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Organelle Crosstalk in Renal Cells: Insights from Cell Biology and Implications for AKI-to-CKD Transition.International journal of molecular sciences · 2026Review
- Mitochondria-ER contact sites (MERCS) in the cell cycle: molecular architecture and functional remodeling across cellular states.BMC biology · 2026Review
- Evaluating the mechanisms and therapeutic potential of ZnO nanoparticles as selective anticancer agents for lung malignancies.Discover nano · 2026Review
- A paradoxical relationship between mitochondrial calcium regulation and retinal ganglion cell degeneration after axon damage.bioRxiv : the preprint server for biology · 2026Article
- Article
- The PVAT-MAMs Axis in Atherosclerosis: A Hypothesis-Driven Cross-Scale Conceptual Framework.International journal of molecular sciences · 2026Review
- Mitochondrial dysfunction in the bovine mammary gland: regulatory mechanisms and therapeutic strategies.Journal of animal science and biotechnology · 2026Review
- Skin capillary endothelial cells form a network of spatiotemporally conserved CabioRxiv : the preprint server for biology · 2026Article
- Mitochondrial Transplantation as a Therapeutic Strategy for Inherited Mitochondrial Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- M2 Macrophages Attenuate AQP2Research (Washington, D.C.) · 2026Article
- Article
175 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
12 authors.
Funding
Abstract
Mitochondria are key decoding stations of the apoptotic process. In support of this view, a large body of experimental evidence has unambiguously revealed that, in addition to the well-established function of producing most of the cellular ATP, mitochondria play a fundamental role in triggering apoptotic cell death. Various apoptotic stimuli cause the release of specific mitochondrial pro-apoptotic factors into the cytosol. The molecular mechanism of this release is still controversial, but there is no doubt that mitochondrial calcium (Ca(2+)) overload is one of the pro-apoptotic ways to induce the swelling of mitochondria, with perturbation or rupture of the outer membrane, and in turn the release of mitochondrial apoptotic factors into the cytosol. Here, we review as different proteins that participate in mitochondrial Ca(2+) homeostasis and in turn modulate the effectiveness of Ca(2+)-dependent apoptotic stimuli. Strikingly, the final outcome at the cellular level is similar, albeit through completely different molecular mechanisms: a reduced mitochondrial Ca(2+) overload upon pro-apoptotic stimuli that dramatically blunts the apoptotic response.
Indexed as
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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.