Eoin obtained a bachelor's degree in Pharmacology (2002) and a PhD (2007) from University College Dublin (UCD). During his postdoctoral career, Eoin became interested in the potential role for carbon dioxide as a modulator of inflammatory and immune signalling, in particular in relation to nuclear factor-κB signalling. The first paper on this work was published in the Journal of Immunology in 2010. In 2013, Eoin obtained his first faculty position as a Lecturer/Assistant Professor in Physiology in the School of Medicine UCD, and he currently leads a research group focused on the effects of hypercapnia on inflammation and immunity.
New Findings r What is the topic of this review?
This review highlights the transcriptional consequences for decreased cellular O 2 levels (hypoxia) and increased cellular CO 2 levels (hypercapnia). r What advances does it highlight?We discuss recent advances in our understanding of the cellular response to hypoxia and consider the potential cross-talk between O 2 -and CO 2 -dependent transcriptional regulation.Oxygen and carbon dioxide are the substrate and product of aerobic metabolism, respectively. Thus, the levels of these physiological gases are inextricably linked in physiological and pathophysiological conditions. Increased mitochondrial consumption of O 2 (to produce ATP) will produce more CO 2 . Furthermore, in lung pathologies such as chronic obstructive pulmonary disease, sleep apnoea and central hypoventilation syndrome, hypoxia and hypercapnia are co-incident. Acute responses to hypoxia involve carotid body-mediated changes in the rate and depth of breathing. Chronic adaptation to hypoxia involves a multitude of changes on a transcriptional level, which simultaneously increases oxygen utilization (via hypoxia-inducible factor and others), while suppressing superfluous energy-demanding processes. Acute responses to CO 2 affect breathing primarily via central chemoreceptors. The nature of hypercapnia-dependent transcriptional regulation is an emerging area of research, but at present the mechanisms underpinning this response are not fully characterized and understood. Thus, given the juxtaposition of hypoxia and hypercapnia in health and disease, this manuscript reviews the current evidence for transcriptional responses to hypoxia and hypercapnia. Finally, we discuss the potential cross-talk between hypoxia and hypercapnia on a transcriptional level.