Dr. Glasier pursues research questions with the overall goal of improving human health, performance and safety during exposure to hyper- and hypobaric environments. Sarcopenia and obesity are conditions whereby oxidative damage and low-grade inflammation are linked to impaired mitochondrial quality control and function. Heme oxygenase-1 (HO-1) induction reduces skeletal muscle oxidant production and inflammation in diet-induce obesity and models of skeletal muscle atrophy. HO-1 is an enzyme system that catalyzes the breakdown of heme, an iron-containing porphyrin and prooxidant, to bilverdin, non-heme iron and carbon monoxide (CO). Bilverdin is rapidly reduced to bilirubin via biliverdin reductase (an antioxidant), and non-heme iron is either stored as ferritin or oxidized by hydrogen peroxide forming oxidants (Fenton reaction). CO is a gas signaling molecule that regulates activation of the transcription factors nuclear factor erythroid 2-related factor 2 (Nrf2), nuclear respiratory factor (NRF)-1 and NRF-2, which coordinately activate antioxidant and inflammatory gene transcription. In addition, HO-1/CO mediated activation of Nrf2 and NRF-1 regulates mitochondrial quality control, the integrated processes of mitochondrial dynamics, mitophagy and biogenesis. It remains unknown whether the skeletal muscle HO-1 enzyme system is impacted in sarcopenic obesity, and contributing to deterioration in mitochondrial population and muscle atrophy. Sources: https://scholars.duke.edu/person/heath.gasier; https://anesthesiology.duke.edu/personnel/heath-gasier-phd-2021
Dr. Glasier pursues research questions with the overall goal of improving human health, performance and safety during exposure to hyper- and hypobaric environments.
Sarcopenia and obesity are conditions whereby oxidative damage and low-grade inflammation are linked to impaired mitochondrial quality control and function. Heme oxygenase-1 (HO-1) induction reduces skeletal muscle oxidant production and inflammation in diet-induce obesity and models of skeletal muscle atrophy. HO-1 is an enzyme system that catalyzes the breakdown of heme, an iron-containing porphyrin and prooxidant, to bilverdin, non-heme iron and carbon monoxide (CO). Bilverdin is rapidly reduced to bilirubin via biliverdin reductase (an antioxidant), and non-heme iron is either stored as ferritin or oxidized by hydrogen peroxide forming oxidants (Fenton reaction). CO is a gas signaling molecule that regulates activation of the transcription factors nuclear factor erythroid 2-related factor 2 (Nrf2), nuclear respiratory factor (NRF)-1 and NRF-2, which coordinately activate antioxidant and inflammatory gene transcription. In addition, HO-1/CO mediated activation of Nrf2 and NRF-1 regulates mitochondrial quality control, the integrated processes of mitochondrial dynamics, mitophagy and biogenesis. It remains unknown whether the skeletal muscle HO-1 enzyme system is impacted in sarcopenic obesity, and contributing to deterioration in mitochondrial population and muscle atrophy.
Sources: https://scholars.duke.edu/person/heath.gasier; https://anesthesiology.duke.edu/personnel/heath-gasier-phd-2021
