ArticleInternational journal of molecular sciences2011
Nifedipine protects INS-1 β-cell from high glucose-induced ER stress and apoptosis.
Article in International journal of molecular sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 44 citations in OpenAlex.
- L-type calcium channel blockade worsens glucose tolerance and β-cell function in C57BL6/J mice exposed to intermittent hypoxia.American journal of physiology. Endocrinology and metabolism · 2025Article
- Nifedipine Improves the Ketogenic Diet Effect on Insulin-Resistance-Induced Cognitive Dysfunction in Rats.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Comparative Analysis of Orthosteric and Allosteric GLP-1R Agonists' Effects on Insulin Secretion from Healthy, Diabetic, and Recovered INS-1E Pancreatic Beta Cells.International journal of molecular sciences · 2024Article
- Endoplasmic reticulum stress: a novel targeted approach to repair bone defects by regulating osteogenesis and angiogenesis.Journal of translational medicine · 2023Review
- Chemical Constituents from the Roots ofPharmaceutics · 2023Article
- Small Molecule-mediated Insulin Hypersecretion Induces Transient ER Stress Response and Loss of Beta Cell Function.Endocrinology · 2022Article
- Dual Beneficial Effects of α-Spinasterol Isolated fromPlants (Basel, Switzerland) · 2022Article
- Elevated triglyceride-glucose (TyG) index predicts impaired islet β-cell function: A hospital-based cross-sectional study.Frontiers in endocrinology · 2022Article
- Why antidiabetic drugs are potentially neuroprotective during the Sars-CoV-2 pandemic: The focus on astroglial UPR and calcium-binding proteins.Frontiers in cellular neuroscience · 2022Review
- Beta-Cell Adaptation to Pregnancy - Role of Calcium Dynamics.Frontiers in endocrinology · 2022Review
- Schisandrin C Affects Glucose-Stimulated Insulin Secretion in Pancreatic β-Cells and Glucose Uptake in Skeletal Muscle Cells.Molecules (Basel, Switzerland) · 2021Article
- Nifedipine Upregulates ATF6-α, Caspases -12, -3, and -7 Implicating Lipotoxicity-Associated Renal ER Stress.International journal of molecular sciences · 2020Article
- The association of calcium channel blockers with β-cell function in type 2 diabetic patients: A cross-sectional study.Journal of clinical hypertension (Greenwich, Conn.) · 2019Article
- Calcium Channel Blockade Ameliorates Endoplasmic Reticulum Stress in the Hippocampus Induced by Amyloidopathy in the Entorhinal Cortex.Iranian journal of pharmaceutical research : IJPR · 2019Article
- Hypoxia induces miR-153 through the IRE1α-XBP1 pathway to fine tune the HIF1α/VEGFA axis in breast cancer angiogenesis.Oncogene · 2018Article
- Calcium channel blockers as drug repurposing candidates for gestational diabetes: Mining large scale genomic and electronic health records data to repurpose medications.Pharmacological research · 2018Article
- Suppression of pancreatic beta cell apoptosis by Danzhi Jiangtang capsule contributes to the attenuation of type 1 diabetes in rats.BMC complementary and alternative medicine · 2016Article
- Protein prenylation in islet β-cell function in health and diabetes: Putting the pieces of the puzzle together.Biochemical pharmacology · 2015Article
- Late sodium current (INaL) in pancreatic β-cells.Pflugers Archiv : European journal of physiology · 2015Article
- Liriodenine induces the apoptosis of human laryngocarcinoma cells via the upregulation of p53 expression.Oncology letters · 2015Article
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
Sustained high concentration of glucose has been verified toxic to β-cells. Glucose augments Ca(2+)-stimulated insulin release in pancreatic β-cells, but chronic high concentration of glucose could induce a sustained level of Ca(2+) in β-cells, which leads to cell apoptosis. However, the mechanism of high glucose-induced β-cell apoptosis remains unclear. In this study, we use a calcium channel blocker, nifedipine, to investigate whether the inhibition of intracellular Ca(2+) concentration could protect β-cells from chronic high glucose-induced apoptosis. It was found that in a concentration of 33.3 mM, chronic stimulation of glucose could induce INS-1 β-cells apoptosis at least through the endoplasmic reticulum stress pathway and 10 μM nifedipine inhibited Ca(2+) release to protect β-cells from high glucose-induced endoplasmic reticulum stress and apoptosis. These results indicated that inhibition of Ca(2+) over-accumulation might provide benefit to attenuate islet β-cell decompensation in a high glucose environment.
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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.