ArticleAmerican journal of physiology. Heart and circulatory physiology2011
Endonuclease G mediates endothelial cell death induced by carbamylated LDL.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Impact of Uremic Toxins on Endothelial Dysfunction in Chronic Kidney Disease: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- Protein carbamylation in atherosclerotic plaques correlates with uremia and disease progression, localizing predominantly to foam cells.Frontiers in immunology · 2025Article
- Drug repositioning of mesalamine via supramolecular nanoassembly for the treatment of drug-induced acute liver failure.Theranostics · 2025Article
- Carbamylated lipoproteins in diabetes.World journal of diabetes · 2023Review
- Mitochondrion-Mediated Cell Death through Erk1-Alox5 Independent of Caspase-9 Signaling.Cells · 2022Article
- DNase I Induces Other Endonucleases in Kidney Tubular Epithelial Cells by Its DNA-Degrading Activity.International journal of molecular sciences · 2020Article
- Association of Endonuclease G Gene Variants with Cardiovascular Disease Risk Factors.Reports of biochemistry & molecular biology · 2019Article
- Estimating the Level of Carbamoylated Plasma Non-High-Density Lipoproteins Using Infrared Spectroscopy.Journal of clinical medicine · 2019Article
- Genome-wide RNAi screen reveals ALK1 mediates LDL uptake and transcytosis in endothelial cells.Nature communications · 2016Article
- Reduction of carbamylated albumin by extended hemodialysis.Hemodialysis international. International Symposium on Home Hemodialysis · 2016Article
- Carbamylated Low-Density Lipoprotein (cLDL)-Mediated Induction of Autophagy and Its Role in Endothelial Cell Injury.PloS one · 2016Article
- Cholesterol Metabolism in CKD.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2015Review
- Regulation of Apoptotic Endonucleases by EndoG.DNA and cell biology · 2015Article
- Novel cytoprotective inhibitors for apoptotic endonuclease G.DNA and cell biology · 2015Article
- Novel high-throughput deoxyribonuclease 1 assay.Journal of biomolecular screening · 2015Article
- Protective effect of zinc-N-acetylcysteine on the rat kidney during cold storage.American journal of physiology. Renal physiology · 2013Article
- CHIP has a protective role against oxidative stress-induced cell death through specific regulation of endonuclease G.Cell death & disease · 2013Article
- Carbamylated-oxidized LDL: proatherosclerotic effects on endothelial cells and macrophages.Journal of atherosclerosis and thrombosis · 2013Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
End-stage kidney disease is a terminal stage of chronic kidney disease, which is associated with a high incidence of cardiovascular disease. Cardiovascular disease frequently results from endothelial injury caused by carbamylated LDL (cLDL), the product of LDL modification by urea-derived cyanate. Our previous data suggested that cLDL induces mitogen-activated protein kinase-dependent mitotic DNA fragmentation and cell death. However, the mechanism of this pathway is unknown. The current study demonstrated that cLDL-induced endothelial mitotic cell death is independent of caspase-3. The expression of endonuclease G (EndoG), the nuclease implicated in caspase-independent DNA fragmentation, was significantly increased in response to cLDL exposure to the cells. The inhibition of EndoG by RNAi protected cLDL-induced DNA fragmentation, whereas the overexpression of EndoG induced more DNA fragmentation in endothelial cells. Ex vivo experiments with primary endothelial cells isolated from wild-type (WT) and EndoG knockout (KO) mice demonstrated that EndoG KO cells are partially protected against cLDL toxicity compared with WT cells. To determine cLDL toxicity in vivo, we administered cLDL or native LDL (nLDL) intravenously to the WT and EndoG KO mice and then measured floating endothelial cells in blood using flow cytometry. The results showed an increased number of floating endothelial cells after cLDL versus nLDL injection in WT mice but not in EndoG KO mice. Finally, the inhibitors of MEK-ERK1/2 and JNK-c-jun pathways decreased cLDL-induced EndoG overexpression and DNA fragmentation. In summary, our data suggest that cLDL-induced endothelial toxicity is caspase independent and results from EndoG-dependent DNA fragmentation.
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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.