ArticleThe Journal of membrane biology2007
Modulation of the permeability transition pore by inhibition of the mitochondrial K(ATP) channel in liver vs. brain mitochondria.
Article in The Journal of membrane biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Explore the key genes and prognosis related to mitochondrial permeability transition driving necrosis gene in kidney renal clear cell carcinoma.Scientific reports · 2025Article
- Mitochondrial Oxidative Stress Is the General Reason for Apoptosis Induced by Different-Valence Heavy Metals in Cells and Mitochondria.International journal of molecular sciences · 2023Review
- Regulation of Mitochondrial Permeability Transition Pore Opening by Monovalent Cations in Liver Mitochondria.International journal of molecular sciences · 2023Article
- Neuroprotective activities of curcumin and quercetin with potential relevance to mitochondrial dysfunction induced by oxaliplatin.Protoplasma · 2016Article
- Closure of mitochondrial potassium channels favors opening of the Tl(+)-induced permeability transition pore in Ca(2+)-loaded rat liver mitochondria.Journal of bioenergetics and biomembranes · 2015Article
- Signal transduction to the permeability transition pore.FEBS letters · 2010Review
- Single channel studies of the ATP-regulated potassium channel in brain mitochondria.Journal of bioenergetics and biomembranes · 2009Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inhibition of the mitochondrial K(ATP) (mitoK(ATP)) channel abrogates the beneficial effects of preconditioning induced by a brief episode of sublethal ischemia. We studied the effect of 5-hydroxydecanoate, a well-known inhibitor of the mitoK(ATP) channel, on swelling of isolated liver and brain mitochondria. Volume changes were determined by measurement of light absorbance at 540 nm. Mitochondrial swelling induced by adding Ca(2+ )ions correlated with opening of the permeability transition pore as shown by modulation by 1 microM cyclosporin A. In brain mitochondria, 5-hydroxydecanoate did not significantly affect Ca(2+)-induced swelling. In contrast, 50 or 500 microM 5-hydroxydecanoate increased swelling of liver mitochondria by 9.7 +/- 5.1% (n = 6, P = 0.057) and 29.4 +/- 1.4% (n = 5, P < 0.0001), respectively. The effect of 5-hydroxydecanoate was blocked by cyclosporin A and was dependent on the presence of potassium in the medium. In medium containing 200 microM ATP to inhibit the mitoK(ATP )channel, 5-hydroxydecanoate did not further increase Ca(2+)-induced swelling. We conclude that inhibition of the mitoK(ATP) channel exerts its detrimental effect by facilitation of permeability transition pore opening.
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