ReviewJournal of clinical immunology1999
Mitochondria and apoptosis: HQ or high-security prison?
Review in Journal of clinical immunology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 54 citations in OpenAlex.
- Anticancer Nanoparticle Carriers of the Proapoptotic Protein CytochromePharmaceutics · 2025Review
- Metallic Nanoparticles: General Research Approaches to Immunological Characterization.Nanomaterials (Basel, Switzerland) · 2018Review
- Flupirtine derivatives as potential treatment for the neuronal ceroid lipofuscinoses.Annals of clinical and translational neurology · 2018Article
- Propolis extracts from the northern region of Thailand suppress cancer cell growth through induction of apoptosis pathways.Investigational new drugs · 2016Article
- Molecular Effects of Irradiation (Cobalt-60) on the Control of Panonychus citri (Acari: Tetranychidae).International journal of molecular sciences · 2015Article
- Transfection of poly(I:C) can induce reactive oxygen species-triggered apoptosis and interferon-β-mediated growth arrest in human renal cell carcinoma cells via innate adjuvant receptors and the 2-5A system.Molecular cancer · 2014Article
- Pro-apoptotic activity of imidazole derivatives mediated by up-regulation of Bax and activation of CAD in Ehrlich Ascites Tumor cells.Investigational new drugs · 2007Article
- Propagation of the apoptotic signal by mitochondrial waves.The EMBO journal · 2001Article
- Cytochrome c maintains mitochondrial transmembrane potential and ATP generation after outer mitochondrial membrane permeabilization during the apoptotic process.The Journal of cell biology · 2001Article
- Cloning and mitochondrial localization of full-length D-AKAP2, a protein kinase A anchoring protein.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- Molecular steps of cell suicide: an insight into immune senescence.Journal of clinical immunology · 2000Review
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Whether we view the mitochondria as the headquarters for the leader of a crack suicide squad or as a prison for the leader of a militant coup, the role of the mitochondria in the apoptotic process is now well established. During apoptosis the integrity of the mitochondria is breeched, the mitochondrial transmembrane potential drops, the electron transport chain is disrupted. and proteins from the mitochondrial intermembrane space (MIS) such as cytochrome c are released into the cytosol, although not necessarily in that order. In the cytosol, cytochrome c forms part of a proteinaceous complex that directly activates caspase-9, one of the apical enzymes responsible for the dismantling of the cell. In this way a mitochondrial factor which is normally locked away from the rest of the cell can directly trigger apoptosis. The need to regulate the release of cytochrome c suggests that the mitochondria may be the decision center for whether a cell lives or dies. Various hypotheses have been formulated to explain how proteins of the MIS are released and how this process is regulated. These include the Bcl-2-regulated opening of a permeability transition pore or an increase in mitochondrial transmembrane potential followed by outer membrane rupture. It remains to be clarified which mitochondria specific events are essential for apoptosis and which are merely consequences of apoptosis.
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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.