ArticleiScience2022
Both ANT and ATPase are essential for mitochondrial permeability transition but not depolarization.
Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 31 citations in OpenAlex.
- Label-free real-time imaging of mitochondrial matrix volume changes and permeability transition in living cells.bioRxiv : the preprint server for biology · 2026Article
- A robust workflow for 3D imaging of human mitochondria using cryo-electron tomography.bioRxiv : the preprint server for biology · 2026Article
- Article
- MRPL13 enhances mitochondrial function and promotes tumor progression in ovarian cancer by inhibiting mPTP opening via SLC25A6.Cell death & disease · 2025Article
- Differential effects of endo- and exopolyphosphatase expression on the induction of the mitochondrial permeability transition pore.Biochimica et biophysica acta. Biomembranes · 2025Article
- Modulation of mitochondrial permeability transition pores in reperfusion injury: Mechanisms and therapeutic approaches.European journal of clinical investigation · 2025Review
- Functional activity and morphology of isolated rat cardiac mitochondria under calcium overload. Effect of naringin.Molecular and cellular biochemistry · 2024Article
- Role of layilin in regulating mitochondria-mediated apoptosis: a study on B cell lymphoma (BCL)-2 family proteins.BMC molecular and cell biology · 2024Article
- The Role of Mitochondrial Permeability Transition in Bone Metabolism, Bone Healing, and Bone Diseases.Biomolecules · 2024Review
- Article
- Tissue-specific differences in CaPhysiological reports · 2024Article
- Inorganic polyphosphate and ion transport across biological membranes.Biochemical Society transactions · 2024Review
- The mitochondrial ATP synthase is a negative regulator of the mitochondrial permeability transition pore.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Article
- Blocking Mitochondrial Pyruvate Transport Alters Corneal Myofibroblast Phenotype: A New Target for Treating Fibrosis.Investigative ophthalmology & visual science · 2023Article
- Identity, structure, and function of the mitochondrial permeability transition pore: controversies, consensus, recent advances, and future directions.Cell death and differentiation · 2023Review
- Mitochondrial Volume Regulation and Swelling Mechanisms in Cardiomyocytes.Antioxidants (Basel, Switzerland) · 2023Review
- Article
- Mitochondrial calcium cycling in neuronal function and neurodegeneration.Frontiers in cell and developmental biology · 2023Review
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An increase in permeability of the mitochondrial inner membrane, mitochondrial permeability transition (PT), is the central event responsible for cell death and tissue damage in conditions such as stroke and heart attack. PT is caused by the cyclosporin A (CSA)-dependent calcium-induced pore, the permeability transition pore (PTP). The molecular details of PTP are incompletely understood. We utilized holographic and fluorescent microscopy to assess the contribution of ATP synthase and adenine nucleotide translocator (ANT) toward PTP. In cells lacking either ATP synthase or ANT, we observed CSA-sensitive membrane depolarization, but not high-conductance PTP. In wild-type cells, calcium-induced CSA-sensitive depolarization preceded opening of PTP, which occurred only after nearly complete mitochondrial membrane depolarization. We propose that both ATP synthase and ANT are required for high-conductance PTP but not depolarization, which presumably occurs through activation of the low-conductance PT, which has a molecular nature that is different from both complexes.
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.