ArticleScientific reports2015
ORMDL3 contributes to the risk of atherosclerosis in Chinese Han population and mediates oxidized low-density lipoprotein-induced autophagy in endothelial cells.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- ORMDL3 as Key Regulator of Endothelial Dysfunction in Atherosclerosis via Sphingolipid Biosynthesis.Inflammation · 2026Article
- Genotype epigenome phenotype integration reveals peripheral immune contributions to type I bipolar disorder.Nature communications · 2026Article
- Review
- ORMDL3 restrains type I interferon signaling and anti-tumor immunity by promoting RIG-I degradation.eLife · 2025Article
- Sphingolipid metabolites involved in the pathogenesis of atherosclerosis: perspectives on sphingolipids in atherosclerosis.Cellular & molecular biology letters · 2025Review
- Fine-tuned protein-lipid interactions in biological membranes: exploration and implications of the ORMDL-ceramide negative feedback loop in the endoplasmic reticulum.Frontiers in cell and developmental biology · 2024Article
- ORMDL in metabolic health and disease.Pharmacology & therapeutics · 2023Review
- The inhibition of ORMDL3 prevents Alzheimer's disease through ferroptosis by PERK/ATF4/HSPA5 pathway.IET nanobiotechnology · 2023Article
- Article
- Asthma Susceptibility GeneAmerican journal of respiratory cell and molecular biology · 2022Article
- Sphingolipid Metabolism and Signaling in Endothelial Cell Functions.Advances in experimental medicine and biology · 2022Review
- ORMDL3 Functions as a Negative Regulator of Antigen-Mediated Mast Cell ActivationFrontiers in immunology · 2021Article
- The protective effects of angelica organic acid against ox-LDL-induced autophagy dysfunction of HUVECs.BMC complementary medicine and therapies · 2020Article
- Ceramide Imbalance and Impaired TLR4-Mediated Autophagy in BMDM of an ORMDL3-Overexpressing Mouse Model.International journal of molecular sciences · 2019Article
- Anti inflammatory effect of asiaticoside on human umbilical vein endothelial cells induced by ox-LDL.Cytotechnology · 2018Article
- Autophagic Regulation of Lipid Homeostasis in Cardiometabolic Syndrome.Frontiers in cardiovascular medicine · 2018Article
- Platelet-rich Plasma Protects HUVECs against oX-LDL-induced Injury.Open medicine (Warsaw, Poland) · 2018Article
- Early origins of asthma (and allergy).Molecular and cellular pediatrics · 2016Review
- ORMDL proteins regulate ceramide levels during sterile inflammation.Journal of lipid research · 2016Article
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ORMDL sphingolipid biosynthesis regulator 3 (ORMDL3) is a universally confirmed susceptibility gene for asthma and has recently emerged as a crucial modulator in lipid metabolism, inflammation and endoplasmic reticulum (ER) stress-the mechanisms also closely involved in atherosclerosis (AS). Here we first presented the evidence of two single nucleotide polymorphisms regulating ORMDL3 expression (rs7216389 and rs9303277) significantly associated with AS risk and the evidence of increased ORMDL3 expression in AS cases compared to controls, in Chinese Han population. Following the detection of its statistical correlation with AS, we further explored the functional relevance of ORMDL3 and hypothesized a potential role mediating autophagy as autophagy is activated upon modified lipid, inflammation and ER stress. Our results demonstrated that in endothelial cells oxidized low-density lipoprotein (ox-LDL) up-regulated ORMDL3 expression and knockdown of ORMDL3 alleviated not only ox-LDL-induced but also basal autophagy. BECN1 is essential for autophagy initiation and silencing of ORMDL3 suppressed ox-LDL-induced as well as basal BECN1 expression. In addition, deletion of ORMDL3 resulted in greater sensitivity to ox-LDL-induced cell death. Taken together, ORMDL3 might represent a causal gene mediating autophagy in endothelial cells in the pathogenesis of AS.
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