ArticleJournal of cellular and molecular medicine2019
Endoplasmic reticulum stress-dependent autophagy inhibits glycated high-density lipoprotein-induced macrophage apoptosis by inhibiting CHOP pathway.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
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- High Density Lipoprotein Reduces Blood Pressure and Protects Spontaneously Hypertensive Rats Against Myocardial Ischemia-Reperfusion Injury in an SR-BI Dependent Manner.Frontiers in cardiovascular medicine · 2022Article
- D4F alleviates the C/EBP homologous protein-mediated apoptosis in glycated high-density lipoprotein-treated macrophages by facilitating autophagy.Experimental biology and medicine (Maywood, N.J.) · 2021Article
- LKB1 Regulates Vascular Macrophage Functions in Atherosclerosis.Frontiers in pharmacology · 2021Review
- Targeting autophagy to overcome drug resistance: further developments.Journal of hematology & oncology · 2020Review
- Erythropoietin Derived Peptide Improved Endoplasmic Reticulum Stress and Ischemia-Reperfusion Related Cellular and Renal Injury.Frontiers in medicine · 2020Article
- Activation of PERK Contributes to Apoptosis and GCancers · 2019Article
- Endoplasmic Reticulum Stress: A Critical Molecular Driver of Endothelial Dysfunction and Cardiovascular Disturbances Associated with Diabetes.International journal of molecular sciences · 2019Review
- Endoplasmic reticulum stress-dependent autophagy inhibits glycated high-density lipoprotein-induced macrophage apoptosis by inhibiting CHOP pathway.Journal of cellular and molecular medicine · 2019Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study was designed to explore the inductive effect of glycated high-density lipoprotein (gly-HDL) on endoplasmic reticulum (ER) stress-C/EBP homologous protein (CHOP)-mediated macrophage apoptosis and its relationship with autophagy. Our results showed that gly-HDL caused macrophage apoptosis with concomitant activation of ER stress pathway, including nuclear translocation of activating transcription factor 6, phosphorylation of protein kinase-like ER kinase (PERK) and eukaryotic translation initiation factor 2α, and CHOP up-regulation, which were inhibited by 4-phenylbutyric acid (PBA, an ER stress inhibitor) and the gene silencing of PERK and CHOP. Similar data were obtained from macrophages treated by HDL isolated from diabetic patients. Gly-HDL induced macrophage autophagy as assessed by up-regulation of beclin-1, autophagy-related gene 5 and microtubule-associated protein one light chain 3-II, which were depressed by PBA and PERK siRNA. Gly-HDL-induced apoptosis, PERK phosphorylation and CHOP up-regulation were suppressed by rapamycin (an autophagy inducer), whereas aggravated by 3-methyladenine (an autophagy inhibitor) and beclin-1 siRNA. Administration of diabetic apoE
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