Thomas Resta

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University of New Mexico School of Medicine

United States

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Dr. Thomas Resta is a Professor at the University of New Mexico School of Medicine, USA. His research focuses on the mechanisms of pulmonary hypertension and acid-sensing ion channels, with recent publications exploring glycolysis, mitochondrial reactive oxygen species, and potential therapeutic targets in the context of hypoxic conditions. Dr. Resta's work contributes significantly to understanding vascular responses and cellular signaling in pulmonary health.

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Vascular Smooth Muscle Signaling in Intermittent Hypoxia-Induced Pulmonary Hypertension

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Articles (15)

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2024

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2020

Collaborators (3)

Nikki Jernigan

Professor

University of New Mexico

UNITED STATES

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Nancy Kanagy

Professor

University of New Mexico School of Medicine

UNITED STATES

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Laura Gonzalez Bosc

Associate Professor

University of New Mexico Health Sciences Center

UNITED STATES

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Thomas Resta

Research Interests

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Recent Grants

Articles (15)

Enhanced glycolysis causes extracellular acidification and activates acid-sensing ion channel 1a in hypoxic pulmonary hypertension

Acid-sensing ion channel 1a activates IKCa/SKCa channels and contributes to endothelium-dependent dilation

Contribution of Mitochondrial Reactive Oxygen Species to Chronic Hypoxia-Induced Pulmonary Hypertension

Hydrogen sulfide and miR21 are suitable biomarkers of hypoxic exposure

Smooth muscle Acid-sensing ion channel 1a as a therapeutic target to reverse hypoxic pulmonary hypertension.

Acid-sensing ion channel 1 contributes to pulmonary arterial smooth muscle cell depolarization following hypoxic pulmonary hypertension.

Acid‐sensing ion channel 1 contributes to pulmonary arterial smooth muscle cell depolarization following hypoxic pulmonary hypertension

Vasoconstrictor Mechanisms in Chronic Hypoxia-Induced Pulmonary Hypertension: Role of Oxidant Signaling.

Membrane depolarization is required for pressure-dependent pulmonary arterial tone but not enhanced vasoconstriction to endothelin-1 following chronic hypoxia.

Coupling of store-operated calcium entry to vasoconstriction is acid-sensing ion channel 1a dependent in pulmonary but not mesenteric arteries

Altered Lipid Domains Facilitate Enhanced Pulmonary Vasoconstriction after Chronic Hypoxia.

Intermittent Hypoxia Augments Pulmonary Vasoconstrictor Reactivity through PKCβ/Mitochondrial Oxidant Signaling.

NFATc3 regulation of collagen V expression contributes to cellular immunity to collagen type V and hypoxic pulmonary hypertension.

Augmented Pulmonary Vasoconstrictor Reactivity after Chronic Hypoxia Requires Src Kinase and Epidermal Growth Factor Receptor Signaling.

PKCβ and reactive oxygen species mediate enhanced pulmonary vasoconstrictor reactivity following chronic hypoxia in neonatal rats.

Collaborators (3)

Nikki Jernigan

Nancy Kanagy

Laura Gonzalez Bosc

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