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Ghazaleh Behnammanesh

Researcher at University of Missouri

Publications -  11
Citations -  213

Ghazaleh Behnammanesh is an academic researcher from University of Missouri. The author has contributed to research in topics: Canagliflozin & Neuroprotection. The author has an hindex of 7, co-authored 8 publications receiving 115 citations. Previous affiliations of Ghazaleh Behnammanesh include Universiti Sains Malaysia.

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Canagliflozin Inhibits Human Endothelial Cell Proliferation and Tube Formation.

TL;DR: Canag liflozin is identified as a robust inhibitor of human EC proliferation and tube formation and the ability of canagliflozin to exert these pleiotropic effects on ECs may contribute to the clinical actions of this drug.
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Canagliflozin inhibits vascular smooth muscle cell proliferation and migration: Role of heme oxygenase-1

TL;DR: It is demonstrated that canagliflozin stimulates the expression of HO-1 in vascular SMCs via the ROS-Nrf2 pathway, and that the induction ofHO-1 contributes to the cellular actions of canag liflozin.
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Effects of Sodium-Glucose Co-Transporter 2 Inhibitors on Vascular Cell Function and Arterial Remodeling.

TL;DR: The role of SGLT2 inhibitors in mediating the vascular actions of these drugs remains to be established as important off-target effects have been identified as discussed by the authors, and future studies distinguishing drug- versus class-specific effects may optimize the selection of specific SGLTs in patients with distinct cardiovascular pathologies.
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Glutaminase-1 stimulates the proliferation, migration, and survival of human endothelial cells.

TL;DR: It is shown that the absence of glutamine in the culture media or the inhibition of GLS1 activity or expression blocked the proliferation and migration of ECs derived from the human umbilical vein, the human aorta, and the human microvasculature.
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Ischemic optic neuropathy as a model of neurodegenerative disorder: A review of pathogenic mechanism of axonal degeneration and the role of neuroprotection.

TL;DR: Various mechanisms involved in the cell loss cascades during axonal degeneration as well as ischemic optic neuropathy are highlighted, including oxidative stress, excitotoxicity, angiogenesis, neuroinflammation and apoptosis following retinal ischemia.