ArticleJournal of atherosclerosis and thrombosis2016
Acid Sphingomyelinase Mediates Oxidized-LDL Induced Apoptosis in Macrophage via Endoplasmic Reticulum Stress.
Article in Journal of atherosclerosis and thrombosis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 34 citations in OpenAlex.
- Heterogeneity of common carotid artery and abdominal aorta: an angle of sphingolipid metabolism in vascular smooth muscle cells.Biomedical engineering online · 2025Article
- The antipsychotic drug thiothixene stimulates macrophages to clear pathogenic cells by inducing arginase 1 and continual efferocytosis.Science signaling · 2025Article
- Neurotensin-neurotensin receptor 2 signaling in adipocytes suppresses food intake through regulating ceramide metabolism.Cell research · 2025Article
- Sphingolipids and Atherosclerosis: The Dual Role of Ceramide and Sphingosine-1-Phosphate.Antioxidants (Basel, Switzerland) · 2023Review
- Desipramine enhances the stability of atherosclerotic plaque in rabbits monitored with molecular imaging.PloS one · 2023Article
- Inflammatory Factors Driving Atherosclerotic Plaque Progression New Insights.Journal of translational internal medicine · 2022Article
- Acid Sphingomyelinase Deficiency: A Clinical and Immunological Perspective.International journal of molecular sciences · 2021Review
- Lipid regulation of NLRP3 inflammasome activity through organelle stress.Trends in immunology · 2021Review
- CD36 Signal Transduction in Metabolic Diseases: Novel Insights and Therapeutic Targeting.Cells · 2021Review
- Bioactive Sphingolipids as Major Regulators of Coronary Artery Disease.Biomolecules & therapeutics · 2021Review
- Role of ASM/Cer/TXNIP signaling module in the NLRP3 inflammasome activation.Lipids in health and disease · 2021Article
- Article
- Nucleotide-binding oligomerization domain protein 2 deficiency enhances CHOP expression and plaque necrosis in advanced atherosclerotic lesions.The FEBS journal · 2020Article
- Endoplasmic reticulum stress-dependent autophagy inhibits glycated high-density lipoprotein-induced macrophage apoptosis by inhibiting CHOP pathway.Journal of cellular and molecular medicine · 2019Article
- Inhibiting Ceramide Synthesis Attenuates Hepatic Steatosis and Fibrosis in Rats With Non-alcoholic Fatty Liver Disease.Frontiers in endocrinology · 2019Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimMacrophage apoptosis is a vital event in advanced atherosclerosis, and oxidized low-density lipoprotein (ox-LDL) is a major contributor to this process. Acid sphingomyelinase (ASM) and ceramide are also involved in the induction of apoptosis, particularly in macrophages. Our current study focuses on ASM and investigates its role in ox-LDL-induced macrophage apoptosis.
methodsHuman THP-1 and mouse peritoneal macrophages were cultured in vitro and treated with ox-LDL. ASM activity and ceramide levels were quantified using ultra performance liquid chromatography. Protein and mRNA levels were analyzed using Western blot analysis and quantitative real-time PCR, respectively. Cell apoptosis was determined using Hoechst staining and flow cytometry.
resultsOx-LDL-induced macrophage apoptosis was triggered by profound endoplasmic reticulum (ER) stress, leading to an upregulation of ASM activity and ceramide levels at an early stage. ASM was inhibited by siRNA or desipramine (DES), and/or ceramide was degraded by recombinant acid ceramidase (AC). These events attenuated the effect of ox-LDL on ER stress. In contrast, recombinant ASM upregulated ceramide and ER stress. ASM siRNA, DES, recombinant AC, and ER stress inhibitor 4-phenylbutyric acid were blocked by elevated levels of C/EBP homologous protein (CHOP); ox-LDL induced elevated levels of CHOP. These events attenuated macrophage apoptosis.
conclusionThese results indicate that ASM/ceramide signaling pathway is involved in ox-LDL-induced macrophage apoptosis via ER stress pathway.
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