Dr. Dennery's focuses on understanding signaling mechanisms involved in hyperoxic lung injury in neonatal models. She has characterized the regulation of heme oxygenase, the rate limiting enzyme in the metabolism of heme. This pathway allows for the degradation of a pro-oxidant molecule and the formation of antioxidant bile pigments and carbon monoxide. She demonstrated that HO-1 which is normally anchored to the smooth endoplasmic reticulum at the C-terminal, can be cleaved under certain conditions to migrate to the nucleus to mediate important signaling functions. She also showed that HO-1 can bind to other proteins such as Nrf2 , the transcription factor that is central to oxidative regulation, to alter downstream signaling. Recently, she has demonstrated that through heme regulation, HO-1 can also modulate circadian rhythmicity in cell models. Recently, using RNA Seq, proteinomics and mathematical modeling, the Dennery laboratory discovered that HO-1 protein can bind to specific DNA sequences, resulting activation of  several transcirption factors. These insights allow for a better understanding of the pleiotropic functions of HO-1.

In addition to the work on HO-1, Dr. Dennery's focus on hyperoxic lung injury in neonates has led to further investigation of the impact of hyperoxia on neonatal metabolism.  Specifically, she identified that hyperoxia alters the glycolytic pathway and leads to altered proliferation and senescence in specific lung cellular subtypes.  Through single cell transcriptomics, she identified that lung macrophages are the predominant cell type that develop senescence in response to hyperoxia. The implications of this on lung injury and repair are the subject of ongoing research.