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Leah R. Villegas

Researcher at University of Colorado Boulder

Publications -  11
Citations -  312

Leah R. Villegas is an academic researcher from University of Colorado Boulder. The author has contributed to research in topics: Hypoxia (medical) & Superoxide dismutase. The author has an hindex of 7, co-authored 11 publications receiving 281 citations. Previous affiliations of Leah R. Villegas include Anschutz Medical Campus & University of Colorado Denver.

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Xanthine Oxidase-Derived ROS Upregulate Egr-1 via ERK1/2 in PA Smooth Muscle Cells; Model to Test Impact of Extracellular ROS in Chronic Hypoxia

TL;DR: An oxidant/antioxidant imbalance arising from loss of EC-SOD in the PA with chronic hypoxia induces Egr-1 via activation of ERK1/2 and contributes to pulmonary vascular remodeling.
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Superoxide Dismutase Mimetic, MnTE-2-PyP, Attenuates Chronic Hypoxia-Induced Pulmonary Hypertension, Pulmonary Vascular Remodeling, and Activation of the NALP3 Inflammasome

TL;DR: This study is the first to demonstrate activation of the NALP3 inflammasome with cleavage of caspase-1 and release of active IL-1 β and IL-18 in chronic hypoxic PH, as well as its attenuation by the SOD mimetic, MnTE-2-PyP.
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Oxidative Stress and Therapeutic Development in Lung Diseases

TL;DR: An overview of Reactive Oxygen Species (ROS) and nitrogen (RNS) species and antioxidants, how they relate to normal physiological function and the pathophysiology of different lung diseases, and therapeutic strategies is provided.
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Selective depletion of vascular EC-SOD augments chronic hypoxic pulmonary hypertension

TL;DR: It is hypothesized that the selective loss of vascular EC-SOD promotes hypoxia-induced PH through redox-sensitive signaling pathways, and deletion of EC- SOD seems to reduce eNOS activity, further compromising pulmonary vascular function.
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Selective Inactivation of PTEN in Smooth Muscle Cells Synergizes With Hypoxia to Induce Severe Pulmonary Hypertension

TL;DR: Chronic inactivation of PTEN selectively in SMC represents a critical mediator of PH progression, leading to cell autonomous events and increased production of factors correlated to proliferation and recruitment of adventitial and inflammatory cells, resulting in irreversible progression of the disease.