ArticleThe Journal of biological chemistry2014
Group VIA phospholipase A2 mitigates palmitate-induced β-cell mitochondrial injury and apoptosis.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 34 citations in OpenAlex.
- Pla2g6 Deficiency Induces Neuronal Precursor Apoptosis During Neurodevelopment.International journal of molecular sciences · 2026Article
- Adaptive mechanisms in pancreatic islets counteract mitochondrial dysfunction in Barth syndrome.Diabetologia · 2026Article
- Phospholipase iPLANature chemical biology · 2021Article
- Lipotoxic Impairment of Mitochondrial Function in β-Cells: A Review.Antioxidants (Basel, Switzerland) · 2021Review
- iPLA2-VIA is required for healthy aging of neurons, muscle, and the female germline in Drosophila melanogaster.PloS one · 2021Article
- Genetic Factors in Antiphospholipid Syndrome: Preliminary Experience with Whole Exome Sequencing.International journal of molecular sciences · 2020Review
- PLA2G6 guards placental trophoblasts against ferroptotic injury.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Metabolic Effects of Selective Deletion of Group VIA Phospholipase ABiomolecules · 2020Article
- Contribution of Oxidative Stress and Impaired Biogenesis of Pancreatic β-Cells to Type 2 Diabetes.Antioxidants & redox signaling · 2019Article
- "Redox lipidomics technology: Looking for a needle in a haystack".Chemistry and physics of lipids · 2019Review
- iPLABiochimica et biophysica acta. Molecular and cell biology of lipids · 2019Review
- Amorphous solid dispersion of Berberine mitigates apoptosis via iPLAInternational journal of biological sciences · 2019Article
- Fatty Acid-Stimulated Insulin Secretion vs. Lipotoxicity.Molecules (Basel, Switzerland) · 2018Review
- Biosynthesis, remodeling and turnover of mitochondrial cardiolipin.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2017Review
- Polarization of Macrophages toward M2 Phenotype Is Favored by Reduction in iPLA2β (Group VIA Phospholipase A2).The Journal of biological chemistry · 2016Article
- Is iPLA2β a Novel Target for the Development of New Strategies to Alleviate Inflammatory Bowel Disease?Digestive diseases and sciences · 2015Article
- Deficiency of Group VIA Phospholipase A2 (iPLA2β) Renders Susceptibility for Chemical-Induced Colitis.Digestive diseases and sciences · 2015Article
- Calcium-independent phospholipases A2 and their roles in biological processes and diseases.Journal of lipid research · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Palmitate (C16:0) induces apoptosis of insulin-secreting β-cells by processes that involve generation of reactive oxygen species, and chronically elevated blood long chain free fatty acid levels are thought to contribute to β-cell lipotoxicity and the development of diabetes mellitus. Group VIA phospholipase A2 (iPLA2β) affects β-cell sensitivity to apoptosis, and here we examined iPLA2β effects on events that occur in β-cells incubated with C16:0. Such events in INS-1 insulinoma cells were found to include activation of caspase-3, expression of stress response genes (C/EBP homologous protein and activating transcription factor 4), accumulation of ceramide, loss of mitochondrial membrane potential, and apoptosis. All of these responses were blunted in INS-1 cells that overexpress iPLA2β, which has been proposed to facilitate repair of oxidized mitochondrial phospholipids, e.g. cardiolipin (CL), by excising oxidized polyunsaturated fatty acid residues, e.g. linoleate (C18:2), to yield lysophospholipids, e.g. monolysocardiolipin (MLCL), that can be reacylated to regenerate the native phospholipid structures. Here the MLCL content of mouse pancreatic islets was found to rise with increasing iPLA2β expression, and recombinant iPLA2β hydrolyzed CL to MLCL and released oxygenated C18:2 residues from oxidized CL in preference to native C18:2. C16:0 induced accumulation of oxidized CL species and of the oxidized phospholipid (C18:0/hydroxyeicosatetraenoic acid)-glycerophosphoethanolamine, and these effects were blunted in INS-1 cells that overexpress iPLA2β, consistent with iPLA2β-mediated removal of oxidized phospholipids. C16:0 also induced iPLA2β association with INS-1 cell mitochondria, consistent with a role in mitochondrial repair. These findings indicate that iPLA2β confers significant protection of β-cells against C16:0-induced injury.
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.