ArticlePloS one2016
Ivabradine Prevents Low Shear Stress Induced Endothelial Inflammation and Oxidative Stress via mTOR/eNOS Pathway.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Low Shear Stress Promotes Atherosclerosis by Mediating Pathological Accumulation of Endothelial Lipid Droplets via the KLF4/TFEB/ATP1A1 Axis.Journal of cardiovascular development and disease · 2026Article
- NO-cGMP Signaling in Endothelial Function of the Healthy and Inflamed Dental Pulp.International journal of molecular sciences · 2025Review
- A Rationale for the Use of Ivabradine in the Perioperative Phase of Cardiac Surgery: A Review.Journal of cardiovascular development and disease · 2025Review
- Article
- Shear stress leads to the dysfunction of endothelial cells through the Cav-1-mediated KLF2/eNOS/ERK signaling pathway under physiological conditions.Open life sciences · 2023Article
- Changes in interstitial fluid flow, mass transport and the bone cell response in microgravity and normogravity.Bone research · 2022Review
- Inflammation of the Human Dental Pulp Induces Phosphorylation of eNOS at Thr495 in Blood Vessels.Biomedicines · 2022Article
- Clinical use of ivabradine in the acute coronary syndrome: A systematic review and narrative synthesis of current evidence.American heart journal plus : cardiology research and practice · 2022Review
- Ivabradine Ameliorates Cardiac Function in Heart Failure with Preserved and Reduced Ejection Fraction via Upregulation of miR-133a.Oxidative medicine and cellular longevity · 2021Article
- Ivabradine and Blood Pressure Reduction: Underlying Pleiotropic Mechanisms and Clinical Implications.Frontiers in cardiovascular medicine · 2021Article
- Integrating Biophysics in Toxicology.Cells · 2020Review
- Detecting the Multiomics Signatures of Factor-Specific Inflammatory Effects on Airway Smooth Muscles.Frontiers in genetics · 2020Article
- Ursolic acid prevents doxorubicin-induced cardiac toxicity in mice through eNOS activation and inhibition of eNOS uncoupling.Journal of cellular and molecular medicine · 2019Article
- Endothelial permeability, LDL deposition, and cardiovascular risk factors-a review.Cardiovascular research · 2018 · on this mapReview
- The Mammalian Target of Rapamycin and DNA methyltransferase 1 axis mediates vascular endothelial dysfunction in response to disturbed flow.Scientific reports · 2017Article
- Shear Stress in Autophagy and Its Possible Mechanisms in the Process of Atherosclerosis.DNA and cell biology · 2017Review
- Impact of Ivabradine on Inflammatory Markers in Chronic Heart Failure.Journal of immunology research · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ivabradine not only reduces heart rate but has other cardiac and vascular protective effects including anti-inflammation and anti-oxidation. Since endothelial nitric oxide synthase (eNOS) is a crucial enzyme in maintaining endothelial activity, we aimed to investigate the impact of ivabradine in low shear stress (LSS) induced inflammation and endothelial injury and the role of eNOS played in it. Endothelial cells (ECs) were subjected to LSS at 2dyne/cm2, with 1 hour of ivabradine (0.04μM) or LY294002 (10μM) pre-treatment. The mRNA expression of IL-6, VCAM-1 along with eNOS were measured by QPCR. Reactive oxygen species (ROS) was detected by dihydroethidium (DHE) and DCF, and protein phosphorylation was detected by western blot. It demonstrated that ivabradine decreased LSS induced inflammation and oxidative stress in endothelial cells. Western blot showed reduced rictor and Akt-Ser473 as well as increased eNOS-Thr495 phosphorylation. However, mTORC1 pathway was only increased when LSS applied within 30 minutes. These effects were reversed by ivabradine. It would appear that ivabradine diminish ROS generation by provoking mTORC2/Akt phosphorylation and repressing mTORC1 induced eNOS-Thr495 activation. These results together suggest that LSS induced endothelial inflammation and oxidative stress are suppressed by ivabradine via mTORC2/Akt activation and mTORC1/eNOS reduction.
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