ArticleDiabetes & vascular disease research
SENP3 regulates high glucose-induced endothelial dysfunction via ROS dependent signaling.
Article in Diabetes & vascular disease research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- SENP3 alleviates osteoporosis via promoting SIRT3 transcription through the increase of DLX2 stability via SUMO2/3.Cell biology and toxicology · 2025Article
- SENP3 mediates the activation of the Wnt/β-catenin signaling pathway to accelerate the growth and metastasis of oesophagal squamous cell carcinoma in mice.Functional & integrative genomics · 2024Article
- Nox4 as a novel therapeutic target for diabetic vascular complications.Redox biology · 2023Review
- Nanocurcumin Reduces High Glucose and Particulate Matter-Induced Endothelial Inflammation: Mitochondrial Function and Involvement of miR-221/222.International journal of nanomedicine · 2023Article
- SENP3 Aggravates Renal Tubular Epithelial Cell Apoptosis in Lipopolysaccharide-Induced Acute Kidney Injury via deSUMOylation of Drp1.Kidney diseases (Basel, Switzerland) · 2022Article
- Effect of Platelet-Derived Growth Factor C on Mitochondrial Oxidative Stress Induced by High d-Glucose in Human Aortic Endothelial Cells.Pharmaceuticals (Basel, Switzerland) · 2022Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe current study aimed to explore the role of SENP3 in endothelial cell dysfunction in a high-glucose setting.
methodsThe gene and protein expressions of SENP3 in high-glucose cultured HAECs were examined using quantitative PCR and western blotting. The effects of SENP3 on HAEC viability, apoptosis, migration, and endothelial-monocyte adhesion were evaluated in vitro by knockdown. Moreover, a mouse streptozotocin-induced type I diabetes model was established for SENP3 expression assessment. In addition, the effects of SENP3 on ROS-related signaling pathways were investigated in high-glucose cultured HAECs.
resultsSignificantly increased levels of SENP3 mRNA and protein were found in high-glucose cultured HAECs in a time-dependent manner. SENP3 knockdown reversed high glucose-induced HAEC viability, apoptosis, and migration reduction. SENP3 knockdown attenuated the high glucose-induced intercellular adhesion of THP-1 monocytic cells and HAECs via downregulation of ICAM-1 and VCAM-1 expression. Increased levels of SENP3, ICAM-1, and VCAM-1 expression were observed in the aorta tissue of mice with type I diabetes. Downregulation of SENP3 expression was observed in HAECs cultured with high glucose levels using the free radical scavenger N-acetyl-L-cysteine or NOX4 siRNA.
conclusionsSENP3 was involved in high glucose-induced endothelial dysfunction, and ROS-dependent signaling served as the mechanism.
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