ArticleCell journal2021
Neutrophil Gelatinase-Associated Lipocalin 2 Accelerates Hypoxia-Induced Endothelial Cell Injury via eNOS/NRF2 Signalling.
Article in Cell journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 5 citations in OpenAlex.
- Perivascular adipokine signaling in abdominal aortic aneurysm: cardiometabolic drivers of vascular remodeling and translational opportunities.Cardiovascular diabetology · 2026Review
- Targeting lipocalin-2 in atherosclerosis: biological functions, pathogenic mechanisms, and therapeutic potential.Frontiers in cardiovascular medicine · 2026Review
- Macula densa nitric oxide synthase 1β restoration by kidney alkalization enhances renal graft outcomes.American journal of physiology. Renal physiology · 2025Article
- Protective Effects of Nerolidol on Thrombotic Events, Systemic Inflammation, Oxidative Stress, and DNA Damage Following Pulmonary Exposure to Diesel Exhaust Particles.Biomedicines · 2025Article
- The Role of Nitric Oxide, Lipocalin-2, and Proinflammatory Cytokines on Proteinuria and Insulin Resistance in Type 2 Diabetes Mellitus Subgroups.International journal of general medicine · 2024Article
- Correlation between neutrophil gelatinase phase lipocalin and cerebral small vessel disease.Frontiers in neurology · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveNeutrophil gelatinase-associated lipocalin (NGAL), a lipocalin, is implicated in many cardiovascular diseases (CVD). The effect of NGAL on endothelial cells (ECs), particularly on ECs injured because of hypoxia, is unclear. In this study, we aim to explore the effect of NGAL in an EC injury in response to hypoxia. MATERIALS AND
methodsIn this experimental study, we isolated and cultured mouse heart ECs (MHECs). The EC injury model was established by exposure of the ECs to hypoxia for 24 hours. The ECs were treated with NGAL (30, 60, 120, 250 and 500 ng/ml). Cell inflammation and oxidative stress were detected by corresponding assays. Apoptotic cells were stained by the terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) assay.
resultsNGAL increased the inflammatory response at the baseline level and further augmented the hypoxia-induced inflammation response. Reactive oxygen species (ROS) levels increased upon NGAL treatment, which caused antioxidase/oxidase imbalance. NGAL also exaggerated hypoxia-induced oxidative stress. The cell apoptosis rate also increased in both the NGAL-treated normoxic and hypoxic conditions. NGAL also reduced endothelial nitric oxide synthase (eNOS)-nitric oxide (NO) signalling, thus decreasing the expression and nuclear translocation of nuclear factor erythroid-2-related factor 2 (NRF2), which was confirmed by overexpression of NRF2.
conclusionNGAL exaggerates EC injury in both normoxic and hypoxic conditions by inhibiting the eNOS-NRF2 pathway.
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