ArticleInternational journal of molecular medicine2018
Exogenous hydrogen sulfide protects human umbilical vein endothelial cells against high glucose‑induced injury by inhibiting the necroptosis pathway.
Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 41 citations in OpenAlex.
- Effect of Huiyang Shengji unguent on the NOD-like receptor family pyrin domain containing protein 3/caspase1/ gasdermin D pathway and lymphatic angiogenesis in patients with diabetic foot ulcer.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026Trial
- Necroptosis and the RIPK1-RIPK3-MLKL pathway in chronic kidney disease: mechanisms, crosstalk, and therapeutic opportunities.Renal failure · 2026Review
- Keratin 18 functions as a lactyltransferase to trigger necroptosis in diabetic kidney disease by modulating Fas transcription.Experimental & molecular medicine · 2026Article
- Orientin Mitigates High Glucose/Ox-LDL-Triggered Endothelial Cell Injury and Atherosclerosis by Regulating MARCH8-Mediated NLRP3 Inflammasome Activation.Mediators of inflammation · 2026Article
- The potential role of hydrogen sulfide-autophagy axis in diseases.Journal of physiology and biochemistry · 2025Review
- Screening of an FDA-Approved Drug Library: Menadione Induces Multiple Forms of Programmed Cell Death in Colorectal Cancer Cells via MAPK8 Cascades.Pharmaceuticals (Basel, Switzerland) · 2025Article
- The role of hydrogen sulfide in the regulation of necroptosis across various pathological processes.Molecular and cellular biochemistry · 2025Review
- Protective Role of HDiabetes, metabolic syndrome and obesity : targets and therapy · 2025Review
- Microvascular destabilization and intricated network of the cytokines in diabetic retinopathy: from the perspective of cellular and molecular components.Cell & bioscience · 2024Review
- Diabetes Mellitus to Accelerated Atherosclerosis: Shared Cellular and Molecular Mechanisms in Glucose and Lipid Metabolism.Journal of cardiovascular translational research · 2024Review
- Exogenous Hydrogen Sulfide Prevents Necroptosis by Inhibiting p38MAPK Pathway Activation in JEG-3 Trophoblast Cells: A Role in Preeclampsia.Gynecologic and obstetric investigation · 2024Article
- Dose-Dependent Effect of Hydrogen Sulfide in Cyclophosphamide-Induced Hepatotoxicity in Rats.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2023Article
- High Glucose-Induced Kidney Injury via Activation of Necroptosis in Diabetic Kidney Disease.Oxidative medicine and cellular longevity · 2023Article
- Exogenous Hydrogen Sulfide Activates PI3K/Akt/eNOS Pathway to Improve Replicative Senescence in Human Umbilical Vein Endothelial Cells.Cardiology research and practice · 2023Article
- Hydrogen sulfide protects against ischemic heart failure by inhibiting RIP1/RIP3/MLKL-mediated necroptosis.Physiological research · 2022Article
- Emerging roles of cystathionine β-synthase in various forms of cancer.Redox biology · 2022Review
- Programmed cell death in atherosclerosis and vascular calcification.Cell death & disease · 2022Review
- Endothelium as a Source and Target of HAntioxidants (Basel, Switzerland) · 2021Review
- Necrostatin-1 and necroptosis inhibition: Pathophysiology and therapeutic implications.Pharmacological research · 2021Review
- Exogenous sodium hydrosulfide protects against high glucose‑induced injury and inflammation in human umbilical vein endothelial cells by inhibiting necroptosis via the p38 MAPK signaling pathway.Molecular medicine reports · 2021Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperglycemia is a key factor in the development of diabetic complications, including the processes of atherosclerosis. Receptor‑interacting protein 3 (RIP3), a mediator of necroptosis, is implicated in atherosclerosis development. Additionally, hydrogen sulfide (H2S) protects the vascular endothelium against hyperglycemia‑induced injury and attenuates atherosclerosis. On the basis of these findings, the present study aimed to confirm the hypothesis that necroptosis mediates high glucose (HG)‑induced injury in human umbilical vein endothelial cells (HUVECs), and that the inhibition of necroptosis contributes to the protective effect of exogenous H2S against this injury. The results revealed that exposure of HUVECs to 40 mM HG markedly enhanced the expression level of RIP3, along with multiple injuries, including a decrease in cell viability, an increase in the number of apoptotic cells, an increase in the expression level of cleaved caspase‑3, generation of reactive oxygen species (ROS), as well as dissipation of the mitochondrial membrane potential (MMP). Treatment of the cells with sodium hydrogen sulfide (NaHS; a donor of H2S) prior to exposure to HG significantly attenuated the increased RIP3 expression and the aforementioned injuries by HG. Notably, treatment of cells with necrostatin‑1 (Nec‑1), an inhibitor of necroptosis, prior to exposure to HG ameliorated the HG‑induced injuries, leading to a decrease in ROS generation and a loss of MMP. However, pre‑treatment of the cells with Nec‑1 enhanced the HG‑induced increase in the expression levels of cleaved caspases‑3 and ‑9. By contrast, pre‑treatment with Z‑VAD‑FMK, a pan ‑caspase inhibitor, promoted the increased expression of RIP3 by HG. Taken together, the findings of the present study have demonstrated, to the best of our knowledge for the first time, that exogenous H2S protects HUVECs against HG‑induced injury through inhibiting necroptosis. The present study has also provided novel evidence that there is a negative interaction between necroptosis and apoptosis in the HG‑treated HUVECs.
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