ReviewDiabetes, obesity & metabolism2010
A link between endoplasmic reticulum stress-induced β-cell apoptosis and the group VIA Ca2+-independent phospholipase A2 (iPLA2β).
Review in Diabetes, obesity & metabolism, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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Who cites it
21 citing papers in PubMed, 46 citations in OpenAlex.
- GPAM mediates mitochondrial dysfunction and the progression of alcoholic liver disease through lipid remodeling.Science advances · 2026Article
- Pla2g6 Deficiency Induces Neuronal Precursor Apoptosis During Neurodevelopment.International journal of molecular sciences · 2026Article
- Heat stress upregulates arachidonic acid to trigger autophagy in sertoli cells via dysfunctional mitochondrial respiratory chain function.Journal of translational medicine · 2024Article
- Regulation of β-cell death by ADP-ribosylhydrolase ARH3 via lipid signaling in insulitis.Cell communication and signaling : CCS · 2024Article
- Alterations in β-Cell Sphingolipid Profile Associated with ER Stress and iPLAMolecules (Basel, Switzerland) · 2021Article
- Metabolic Effects of Selective Deletion of Group VIA Phospholipase ABiomolecules · 2020Article
- Cigarette smoke exposure impairs β-cell function through activation of oxidative stress and ceramide accumulation.Molecular metabolism · 2020Article
- Macrophage polarization is linked to CaJournal of lipid research · 2020Article
- Regulation of Serum Sphingolipids in Andean Children Born and Living at High Altitude (3775 m).International journal of molecular sciences · 2019Article
- Fatty Acid-Induced Lipotoxicity in Pancreatic Beta-Cells During Development of Type 2 Diabetes.Frontiers in endocrinology · 2018Review
- Adiponectin and its Hydrolase-Activated Receptors.Journal of nature and science · 2017Article
- Sphingolipid regulators of cellular dysfunction in Type 2 diabetes mellitus: a systems overview.Clinical lipidology · 2014Article
- Glucolipotoxicity impairs ceramide flow from the endoplasmic reticulum to the Golgi apparatus in INS-1 β-cells.PloS one · 2014Article
- Article
- Role of calcium-independent phospholipase A(2)β in human pancreatic islet β-cell apoptosis.American journal of physiology. Endocrinology and metabolism · 2012Article
- Roles of acidic phospholipids and nucleotides in regulating membrane binding and activity of a calcium-independent phospholipase A2 isoform.The Journal of biological chemistry · 2012Article
- Orai1 calcium channels in the vasculature.Pflugers Archiv : European journal of physiology · 2012Review
- Effects of antagonists and heat on TRPM8 channel currents in dorsal root ganglion neuron activated by nociceptive cold stress and menthol.Neurochemical research · 2012Article
- 15,16-Dihydrotanshinone I, a Compound of Salvia miltiorrhiza Bunge, Induces Apoptosis through Inducing Endoplasmic Reticular Stress in Human Prostate Carcinoma Cells.Evidence-based complementary and alternative medicine : eCAM · 2011Article
- The Role of Phospholipase A(2)-derived Mediators in Obesity.Drug discovery today. Disease mechanisms · 2010Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Endoplasmic reticulum (ER) stress is becoming recognized as an important contributing factor in various diseases, including diabetes mellitus. Prolonged ER stress can cause β-cell apoptosis; however, the underlying mechanism(s) that contribute to this process are not well understood. Early reports suggested that arachidonic acid metabolites and a Ca(2+)-independent phospholipase A(2) (iPLA(2)) activity play a role in β-cell apoptosis. The PLA(2) family of enzymes catalyse the hydrolysis of the sn-2 substituent (i.e. arachidonic acid) of membrane phospholipids. In light of our findings that the pancreatic islet β-cells are enriched in arachidonate-containing phospholipids and express the group VIA iPLA(2)β, we considered the possibility that iPLA(2)β participates in ER stress-induced β-cell apoptosis. Our work revealed a novel mechanism, involving ceramide generation and triggering of mitochondrial abnormalities, by which iPLA(2)β participates in the β-cell apoptosis process. Here, we review our evidence linking ER stress, β-cell apoptosis and iPLA(2)β. Continued studies in this area will increase our understanding of the contribution of iPLA(2)β to the evolution of diabetes mellitus and will further our knowledge of factors that influence β-cell health in diabetes mellitus and identify potential targets for future therapeutic interventions to prevent β-cell death.
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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.