Emma J. Hodson

TL;DR: The clinical presentation of COVID-19 due to infection with SARS-CoV-2 is highly variable with the majority of patients having mild symptoms while others develop severe respiratory failure.

TL;DR: In this article, a comparative analysis of inducible and constitutive inactivation of PHD2 and its principal targets HIF1α and HIF2α was presented.

TL;DR: It is demonstrated that hypoxia and the HIF prolyl hydroxylase inhibitor Roxadustat reduce ACE2 expression and inhibit SARS-CoV-2 entry and replication in lung epithelial cells via a HIF-1α dependent signalling pathway, showing that post-entry steps in the viral life cycle are oxygen-sensitive.

TL;DR: Investigation of the role of HIF prolyl hydroxylase (PHD) enzymes in ventilatory acclimatisation and carotid body biology finds that PHD2+/−, but not PHD1−/− or PHD3−/ −, mice mimic chronic hypoxia in exhibiting exaggerated ventilatories responses to acute hypoxaemia.

TL;DR: Two tricyclic triazole-containing compounds are reported as potent and selective PHD inhibitors which compete with the 2-oxoglutarate co-substrate and one compound induces HIFα in cells and in wildtype mice with marked induction in the brain tissue, revealing that it is useful for studies aimed at validating the upregulation of HIF for treatment of cerebral diseases including stroke.