ArticleCellular signalling2014
Early NADPH oxidase-2 activation is crucial in phenylephrine-induced hypertrophy of H9c2 cells.
Article in Cellular signalling, 2014. 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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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Exogenous L6 myotube mitochondrial transplantation attenuates hypertrophy and elicits a unique proteomic signature in phenylephrine-treated H9C2 cardiomyocytes.bioRxiv : the preprint server for biology · 2026Article
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- NOX Family: Regulators of Reactive Oxygen Species Balance in Tumor Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Natural Bioactive Compounds Targeting NADPH Oxidase Pathway in Cardiovascular Diseases.Molecules (Basel, Switzerland) · 2023Review
- Specific inhibition of NADPH oxidase 2 modifies chronic epilepsy.Redox biology · 2022Article
- Downregulation of PPARα during Experimental Left Ventricular Hypertrophy Is Critically Dependent on Nox2 NADPH Oxidase Signalling.International journal of molecular sciences · 2020Article
- p47phox-Dependent Reactive Oxygen Species Stimulate Nuclear Translocation of the FoxO1 Transcription Factor During Metabolic Inhibition in Cardiomyoblasts.Cell biochemistry and biophysics · 2018Article
- 2-aminoethoxydiphenyl borate provides an anti-oxidative effect and mediates cardioprotection during ischemia reperfusion in mice.PloS one · 2017Article
- Prostanoid-mediated contractions of the carotid artery become Nox2-independent with aging.Age (Dordrecht, Netherlands) · 2015Article
- Nox Inhibitors & Therapies: Rational Design of Peptidic and Small Molecule Inhibitors.Current pharmaceutical design · 2015Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Reactive oxygen species (ROS) produced by different NADPH oxidases (NOX) play a role in cardiomyocyte hypertrophy induced by different stimuli, such as angiotensin II and pressure overload. However, the role of the specific NOX isoforms in phenylephrine (PE)-induced cardiomyocyte hypertrophy is unknown. Therefore we aimed to determine the involvement of the NOX isoforms NOX1, NOX2 and NOX4 in PE-induced cardiomyocyte hypertrophy. Hereto rat neonatal cardiomyoblasts (H9c2 cells) were incubated with 100 μM PE to induce hypertrophy after 24 and 48h as determined via cell and nuclear size measurements using digital imaging microscopy, electron microscopy and an automated cell counter. Digital-imaging microscopy further revealed that in contrast to NOX1 and NOX4, NOX2 expression increased significantly up to 4h after PE stimulation, coinciding and co-localizing with ROS production in the cytoplasm as well as the nucleus. Furthermore, inhibition of NOX-mediated ROS production with apocynin, diphenylene iodonium (DPI) or NOX2 docking sequence (Nox2ds)-tat peptide during these first 4h of PE stimulation significantly inhibited PE-induced hypertrophy of H9c2 cells, both after 24 and 48h of PE stimulation. These data show that early NOX2-mediated ROS production is crucial in PE-induced hypertrophy of H9c2 cells.
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Registered trials
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