ArticleAnatomical record (Hoboken, N.J. : 2007)2012
Mitochondrial swelling and incipient outer membrane rupture in preapoptotic and apoptotic cells.
Article in Anatomical record (Hoboken, N.J. : 2007), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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.
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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
44 citing papers in PubMed.
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- Membrane-camouflaged nanoparticle alleviates intervertebral disc degeneration via oxidative stress suppression and autophagy activation.Materials today. Bio · 2026Article
- FAM162A Is a Key Regulator of Mitochondrial Structure, Dynamics, and Bioenergetics, Driving Cellular Protection and Longevity.Aging cell · 2026Article
- Fundamental mechanism of ferroptosis: Three unanswered questions.Ferroptosis and oxidative stress · 2026Article
- Mitochondrial DNA in systemic lupus erythematosus: pathogenic mechanisms, clinical biomarkers, and precision therapeutic strategies.Frontiers in immunology · 2026Review
- LDL Exposure Disrupts Mitochondrial Function and Dynamics in a Hippocampal Neuronal Cell Line.Molecular neurobiology · 2025Article
- Pregnancy Disorders: A Potential Role for Mitochondrial Altered Homeostasis.Antioxidants (Basel, Switzerland) · 2024Review
- Mechanisms of drug resistance in nutrient-depleted colorectal cancer cells: insights into lysosomal and mitochondrial drug sequestration.Biology open · 2024Review
- Article
- The Interplay between Mitochondrial Dysfunction and Ferroptosis during Ischemia-Associated Central Nervous System Diseases.Brain sciences · 2023Review
- Placental Mitochondrial Function and Dysfunction in Preeclampsia.International journal of molecular sciences · 2023Review
- Article
- The Feline Calicivirus Leader of the Capsid Protein Has the Functional Characteristics of a Viroporin.Viruses · 2022Article
- Mitochondria as a target and central hub of energy division during cold stress in insects.Frontiers in zoology · 2022Review
- Iron insufficiency in floral buds impairs pollen development by disrupting tapetum function.The Plant journal : for cell and molecular biology · 2021Article
- Dynamic changes in mitochondrial 3D structure during folliculogenesis and luteal formation in the goat large luteal cell lineage.Scientific reports · 2021Article
- Article
- Histological changes in placental rat apoptosis via FasL and cytochromeSaudi journal of biological sciences · 2021Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Outer mitochondrial membrane (OMM) rupture was first noted in isolated mitochondria in which the inner mitochondrial membrane (IMM) had lost its selective permeability. This phenomenon referred to as mitochondrial permeability transition (MPT) refers to a permeabilized inner membrane that originates a large swelling in the mitochondrial matrix, which distends the outer membrane until it ruptures. Here, we have expanded previous electron microscopic observations that in apoptotic cells, OMM rupture is not caused by a membrane stretching promoted by a markedly swollen matrix. It is shown that the widths of the ruptured regions of the OMM vary from 6 to 250 nm. Independent of the perforation size, herniation of the mitochondrial matrix appeared to have resulted in pushing the IMM through the perforation. A large, long focal herniation of the mitochondrial matrix, covered with the IMM, was associated with a rupture of the OMM that was as small as 6 nm. Contextually, the collapse of the selective permeability of the IMM may precede or follow the release of the mitochondrial proteins of the intermembrane space into the cytoplasm. When the MPT is a late event, exit of the intermembrane space proteins to the cytoplasm is unimpeded and occurs through channels that transverse the outer membrane, because so far, the inner membrane is impermeable. No channel within the outer membrane can expose to the cytoplasm a permeable inner membrane, because it would serve as a conduit for local herniation of the mitochondrial matrix.
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