ArticleBMC research notes2017
Arginase-I enhances vascular endothelial inflammation and senescence through eNOS-uncoupling.
Article in BMC research notes, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- Molecular determinants of thromboinflammatory activation in inflammatory bowel disease.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Article
- Cinnamon consumption during aerobic training in streptozotocin-nicotinamide-induced type 2 diabetic rats modulates the arginase/eNOS enzyme balance in the soleus muscle and reduces blood glucose levels.BMC sports science, medicine & rehabilitation · 2025Article
- SCIG: Machine learning uncovers cell identity genes in single cells by genetic sequence codes.Nucleic acids research · 2025Article
- Pathophysiology of Arginases in Cancer and Efforts in Their Pharmacological Inhibition.International journal of molecular sciences · 2024Review
- Targeting Cellular Senescence in Aging and Age-Related Diseases: Challenges, Considerations, and the Emerging Role of Senolytic and Senomorphic Therapies.Aging and disease · 2024Review
- Role ofBiomedicines · 2024Review
- Association between the Polymorphisms rs2070744, 4b/a and rs1799983 of theMedicina (Kaunas, Lithuania) · 2023Article
- Uncoupled nitric oxide synthase activity promotes colorectal cancer progression.Frontiers in oncology · 2023Article
- Arginase: shedding light on the mechanisms and opportunities in cardiovascular diseases.Cell death discovery · 2022Review
- Immune Function of Endothelial Cells: Evolutionary Aspects, Molecular Biology and Role in Atherogenesis.International journal of molecular sciences · 2022Review
- Increased expression of miR-224-5p in circulating extracellular vesicles of patients with reduced coronary flow reserve.BMC cardiovascular disorders · 2022Article
- Nintedanib ameliorates oxidized low-density lipoprotein -induced inflammation and cellular senescence in vascular endothelial cells.Bioengineered · 2022Article
- Global research trends in atherosclerosis: A bibliometric and visualized study.Frontiers in cardiovascular medicine · 2022Article
- Article
- Sustained Maternal Smoking Triggers Endothelial-Mediated Oxidative Stress in the Umbilical Cord Vessels, Resulting in Vascular Dysfunction.Antioxidants (Basel, Switzerland) · 2021Article
- Increased immunosuppression impairs tissue homeostasis with aging and age-related diseases.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Arginase impedes the resolution of colitis by altering the microbiome and metabolome.The Journal of clinical investigation · 2020Article
- Arginase inhibition by (-)-Epicatechin reverses endothelial cell aging.European journal of pharmacology · 2020Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAugmented arginase-II (Arg-II) is implicated in endothelial senescence and inflammation through a mutual positive regulatory circuit with S6K1. This study was conducted to investigate whether Arg-I, another isoform of arginase that has been also reported to play a role in vascular endothelial dysfunction, promotes endothelial senescence through similar mechanisms.
resultsThe non-senescent human endothelial cells from umbilical veins (passage 2 to 4) were transduced with empty recombinant adenovirus vector (rAd/CMV) as control or rAd/CMV-Arg-I to overexpress Arg-I. Overexpressing Arg-I promoted eNOS-uncoupling, enhanced senescence markers including p53-S15, p21 and senescence-associated β-galactosidase (SA-β-gal) staining, and increased inflammatory vascular adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) as well as monocyte adhesion to endothelial cells without activating S6K1. All the effects of Arg-I were inhibited by the anti-oxidant N-acetylcysteine (NAC).
conclusionsOur study demonstrates that Arg-I promotes endothelial senescence and inflammatory responses through eNOS-uncoupling unrelated to activation of the S6K1 pathway.
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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.