ArticleOxidative medicine and cellular longevity2021
H9c2 Cardiomyocytes under Hypoxic Stress: Biological Effects Mediated by Sentinel Downstream Targets.
Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 18 citations in OpenAlex.
- Additive effect of Ruta graveolens bioactive phytoconstituents and cisplatin through PKC/MEK/ERK pathway in glioblastoma.Molecular therapy. Oncology · 2026Article
- Metabolic reprogramming enhances oxidative stress resistance in differentiating cardiomyocytes.Scientific reports · 2026Article
- FKBP prolyl isomerase 4: a potential target for heart failure and cardioprotective effects via leonurine-pretreated mesenchymal stem cell-derived exosomes.Stem cell research & therapy · 2025Article
- Transcriptome Analysis of Myocardial Ischemic-Hypoxic Injury in Rats and Hypoxic H9C2 Cells.ESC heart failure · 2024Article
- Comparison of the efficiency of ultrafiltration, precipitation, and ultracentrifugation methods for exosome isolation.Biochemistry and biophysics reports · 2024Article
- Proteomic investigation of acute and chronic hypoxia/reoxygenation responsive proteins and pathways in H9C2 cardiomyoblasts.Turkish journal of biology = Turk biyoloji dergisi · 2024Article
- Cardioprotective Role ofCardiovascular & hematological agents in medicinal chemistry · 2024Article
- From nitrate to NO: potential effects of nitrate-reducing bacteria on systemic health and disease.European journal of medical research · 2023Review
- Desmin Reorganization by Stimuli Inducing Oxidative Stress and Electrophiles: Role of Its Single Cysteine Residue.Antioxidants (Basel, Switzerland) · 2023Article
- Protective Effect of Resveratrol against Hypoxia-Induced Neural Oxidative Stress.Journal of personalized medicine · 2022Article
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The association between diabetes and cardiovascular diseases is well known. Related diabetes macro- and microangiopathies frequently induce hypoxia and consequently energy failure to satisfy the jeopardized myocardium basal needs. Additionally, it is widely accepted that diabetes impairs endothelial nitric oxide synthase (eNOS) activity, resulting in diminished nitric oxide (NO) bioavailability and consequent endothelial cell dysfunction. In this study, we analyzed the embryonic heart-derived H9c2 cell response to hypoxic stress after administration of a high glucose concentration to reproduce a condition often observed in diabetes. We observed that 24 h hypoxia exposure of H9c2 cells reduced cell viability compared to cells grown in normoxic conditions. Cytotoxicity and early apoptosis were increased after exposure to high glucose administration. In addition, hypoxia induced a RhoA upregulation and a Bcl-2 downregulation and lowered the ERK activation observed in normoxia at both glucose concentrations. Furthermore, a significant cell proliferation rate increases after the 1400 W iNOS inhibitor administration was observed. Again, hypoxia increased the expression level of myogenin, a marker of skeletal muscle cell differentiation. The cardiomyocyte gene expression profiles and morphology changes observed in response to pathological
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