ArticleJournal of bioenergetics and biomembranes2004
Ceramide induces release of pro-apoptotic proteins from mitochondria by either a Ca2+ -dependent or a Ca2+ -independent mechanism.
Article in Journal of bioenergetics and biomembranes, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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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Who cites it
22 citing papers in PubMed, 51 citations in OpenAlex.
- Sphingolipid metabolism and regulated cell death in malignant melanoma.Apoptosis : an international journal on programmed cell death · 2024Review
- Emerging Roles of Ceramides in Breast Cancer Biology and Therapy.International journal of molecular sciences · 2022Review
- Lipotoxic very-long-chain ceramides cause mitochondrial dysfunction, oxidative stress, and cell death in cardiomyocytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Ceramide and Ischemia/Reperfusion Injury.Journal of lipids · 2018Review
- Regulation of ceramide channel formation and disassembly: Insights on the initiation of apoptosis.Saudi journal of biological sciences · 2015Article
- Mitochondrial stress signaling promotes cellular adaptations.International journal of cell biology · 2014Review
- Calcium and mitochondrial metabolism in ceramide-induced cardiomyocyte death.Biochimica et biophysica acta · 2013Article
- Sphingolipids in obesity, type 2 diabetes, and metabolic disease.Handbook of experimental pharmacology · 2013Review
- Fatty Acid Oxidation and Cardiovascular Risk during Menopause: A Mitochondrial Connection?Journal of lipids · 2012Article
- Novel pathway of ceramide production in mitochondria: thioesterase and neutral ceramidase produce ceramide from sphingosine and acyl-CoA.The Journal of biological chemistry · 2011Article
- Ceramide and mitochondria in ischemic brain injury.International journal of biochemistry and molecular biology · 2011Article
- Nicotinamide rescues human embryonic stem cell-derived neuroectoderm from parthanatic cell death.Stem cells (Dayton, Ohio) · 2009Article
- Ceramide and mitochondria in ischemia/reperfusion.Journal of cardiovascular pharmacology · 2009Review
- Long-chain ceramide is a potent inhibitor of the mitochondrial permeability transition pore.The Journal of biological chemistry · 2008Article
- Cardiac remodeling in obesity.Physiological reviews · 2008Review
- Anti-apoptotic Bcl-2 Family Proteins Disassemble Ceramide Channels.The Journal of biological chemistry · 2008Article
- Effect of ceramide N-acyl chain and polar headgroup structure on the properties of ordered lipid domains (lipid rafts).Biochimica et biophysica acta · 2007Article
- A house divided: ceramide, sphingosine, and sphingosine-1-phosphate in programmed cell death.Biochimica et biophysica acta · 2006Review
- In vivo administration of D609 leads to protection of subsequently isolated gerbil brain mitochondria subjected to in vitro oxidative stress induced by amyloid beta-peptide and other oxidative stressors: relevance to Alzheimer's disease and other oxidative stress-related neurodegenerative disorders.Free radical biology & medicine · 2006Article
- Sphingosine, a product of ceramide hydrolysis, influences the formation of ceramide channels.Biophysical journal · 2006Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several observations have been reported in the last years indicating that ceramide may activate the mitochondrial route of apoptosis. We show here that on addition of either C2- or C16-ceramide to mitochondria isolated from rat heart and suspended in a saline medium, release of cytochrome c and apoptosis-inducing factor (AIF) from the intermembrane space takes place. The release process is Ca2+ -independent and is not inhibited by Cyclosporin A (CsA). For the protein release process to occur, the presence of an oxidizable substrate is required. When mitochondria are suspended in sucrose instead of potassium medium, only short chain C2-ceramide causes cytochrome c release through a Ca2+ -dependent and CsA sensitive mitochondrial permeability transition (MPT) mechanism. The latter effect appears to be related to the membrane potential dissipating ability exhibited by short chain C2-ceramide.
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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.