ArticleMolecular medicine reports2018
High expression of active ATF6 aggravates endoplasmic reticulum stress‑induced vascular endothelial cell apoptosis through the mitochondrial apoptotic pathway.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
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- Nobiletin enhances Doxorubicin sensitivity in osteosarcoma through ER stress-induced apoptosis mediated by the PI3K/AKT pathway.Scientific reports · 2026Article
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- Decoding interaction between mitochondria and endoplasmic reticulum in ischemic myocardial injury: targeting natural medicines.Frontiers in pharmacology · 2025Review
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- Endoplasmic reticulum stress: a novel targeted approach to repair bone defects by regulating osteogenesis and angiogenesis.Journal of translational medicine · 2023Review
- Non-coding RNA mediates endoplasmic reticulum stress-induced apoptosis in heart disease.Heliyon · 2023Review
- Ultrastructural and Molecular Investigation on Peripheral Leukocytes in Alzheimer's Disease Patients.International journal of molecular sciences · 2023Article
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- Regulation of cardiac fibroblast cell death by unfolded protein response signaling.Frontiers in physiology · 2023Review
- High Glycemia and Soluble Epoxide Hydrolase in Females: Differential Multiomics in Murine Brain Microvasculature.International journal of molecular sciences · 2022Article
- Endoplasmic Reticulum Stress Underlies Nanosilver-Induced Neurotoxicity in Immature Rat Brain.International journal of molecular sciences · 2022Article
- Endoplasmic Reticulum Stress and Pathogenesis of Vascular Calcification.Frontiers in cardiovascular medicine · 2022Review
- Endoplasmic Reticulum Stress of Gut Enterocyte and Intestinal Diseases.Frontiers in molecular biosciences · 2022Review
- 5-Aminolevulinic Acid Attenuates Glucose-Regulated Protein 78 Expression and Hepatocyte Lipoapoptosis via Heme Oxygenase-1 Induction.International journal of molecular sciences · 2021Article
- Endoplasmic Reticulum-Mitochondria Contacts: A Potential Therapy Target for Cardiovascular Remodeling-Associated Diseases.Frontiers in cell and developmental biology · 2021Review
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activating transcription factor 6 (ATF6), one of three sensor proteins in the endoplasmic reticulum (ER), is an important regulatory factor in the ER stress‑induced apoptosis pathway. Although recent studies have made some progress in elucidating the regulation mechanism of ATF6, the specific regulatory mechanism of ER stress‑induced vascular endothelial cell (VEC) apoptosis is still unclear. The present study was designed to investigate the role of ATF6 in VECs under thapsigargin (TG)‑induced ER stress. ATF6 (1‑366aa; ATF6 high‑expressed plasmid) and ATF6 (151‑366aa; plasmid without transcriptional activity) were transfected into VECs to yield an ATF6 high‑expression model and a positive control model, respectively. High expression of ATF6 decreased viability and aggravated ER stress‑induced apoptosis in VECs. Increased expression of apoptosis‑related genes, including those encoding caspase‑3, caspase‑9, C/EBP homologous protein (CHOP), cytochrome c and B‑cell lymphoma‑associated protein X (Bax)/B‑cell lymphoma (Bcl‑)2, was detected by polymerase chain reaction and western blotting in the ATF6 (1‑366aa) + TG group. No significant effect of TG treatment and high ATF6 expression was indicated on the expression of death receptor‑related genes, including those encoding caspase‑8 and Fas. The results demonstrated that high expression of activated ATF6 aggravates ER stress‑induced VEC apoptosis through the mitochondrial apoptotic pathway. Furthermore, in response to ER stress, ATF6 upregulates the expression of caspase‑3, caspase‑9, CHOP, cytochrome c and Bax/Bcl‑2.
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