Broadly speaking, our research focuses on the fascinating and complex physiological responses to hypoxia.
Sustained hypoxia has long been used to model chronic cardiovascular and pulmonary disease, as well as high altitude exposure, although most studies have only looked at the in vivo consequences of very severe hypoxia, like an FiO2 of 0.10 or so. In mice, this leads to oxyhemoglobin saturations in the 60s or 70s, so unfortunately it doesn't properly model realistic human disease. Our data suggest that even slight changes to FiO2 result in very different physiological effects. This is an underexplored area.
Similarly, intermittent hypoxia, as a model of obstructive sleep apnea (OSA), results in metabolic dysfunction, hepatic oxidative stress, atherosclerosis, and other maladaptive phenomena. These studies have typically looked at severe intermittent hypoxia, which accurately models only a small percentage of patients with OSA. Less severe intermittent hypoxia is less well understood. And combining sustained and intermittent hypoxia in mouse models is an area which we are keen to explore further.
We hope to answer so many questions about the relationship of hypoxia to human disease:
What is the impact of obesity in the hypoxia of overlap syndrome?
How does HIF-1 impact physiological outcomes in intermittent and overlap hypoxia?
Does moderate hypoxia impact lung injury in COVID-19? (Should we intubate patients earlier?)
Does the intermittent hypoxia of OSA worsen lung injury in COVID-19?
What is the effect of time restricted feeding on dysglycemia induced by intermittent hypoxia?