# Phyllis A. Dennery
Phyllis A. Dennery is an American physician-scientist in neonatology and lung biology who is the Sylvia Kay Hassenfeld Professor and chair of pediatrics at the Warren Alpert Medical School of Brown University, pediatrician-in-chief at [Rhode Island Hospital](https://www.edgepedia.org/rhode-island-hospital), and medical director of Hasbro Children's Hospital, and who is a member of the [National Academy of Medicine](https://www.edgepedia.org/national-academy-of-medicine).[1](https://www.ncbi.nlm.nih.gov/books/NBK621992/) Her laboratory has studied mechanisms of neonatal lung injury and repair, specifically bronchopulmonary dysplasia (BPD), for over 35 years, focusing on how oxidative stress from supplemental oxygen alters lung development.[2](https://vivo.brown.edu/display/pdennery) She is also professor of molecular biology, cell biology, and biochemistry at Brown.[1](https://www.ncbi.nlm.nih.gov/books/NBK621992/)
| Fact | Detail |
| --- | --- |
| Current roles | Chair of pediatrics, Brown; pediatrician-in-chief, Rhode Island Hospital; medical director, Hasbro Children's Hospital[1](https://www.ncbi.nlm.nih.gov/books/NBK621992/) |
| Research focus | Neonatal hyperoxic lung injury, oxidative stress, and bronchopulmonary dysplasia[3](https://www.nationalacademies.org/projects/HMD-HCS-24-07/download-bios) |
| Career length in lab science | Over 35 years of BPD-focused laboratory research[2](https://vivo.brown.edu/display/pdennery) |
| NIH funding | Continuously NIH-funded for 24 years as of her 2015 Brown recruitment[4](https://archive2.news.brown.edu/2007-2015/articles/2014/10/dennery.html) |
| Major honors | National Academy of Medicine (2014); Association of American Physicians (2015); American Thoracic Society fellow (2022)[2](https://vivo.brown.edu/display/pdennery) |
| Key mechanistic finding | Early programmed senescence supports lung development, while later hyperoxia-induced senescence (p53/p21 pathway) drives injury[5](https://doi.org/10.1038/s41467-023-35985-4) |
| National service | Co-chair, National Academies committee on enhancing NIH-funded pediatric health research (2024–2025)[3](https://www.nationalacademies.org/projects/HMD-HCS-24-07/download-bios) |
## Education and training
Dennery earned her B.S. in biology from [McGill University](https://www.edgepedia.org/mcgill-university) and her medical degree from [Howard University](https://www.edgepedia.org/howard-university). She completed a residency in pediatrics at Children's Hospital National Medical Center in Washington, DC, and a fellowship in neonatology at [Case Western Reserve University](https://www.edgepedia.org/case-western-reserve-university).[1](https://www.ncbi.nlm.nih.gov/books/NBK621992/)
## Career
Dennery held roles at Stanford University as director of neonatology research and associate division chief. There she studied heme oxygenase-1 (HO-1) in lung anti-oxidative defenses and, with collaborators, defined HO-1's function as a signaling molecule independent of its enzymatic activity and described its migration from the smooth endoplasmic reticulum to the nucleus.[2](https://vivo.brown.edu/display/pdennery)
She then served as division chief in neonatology at [Children's Hospital of Philadelphia](https://www.edgepedia.org/childrens-hospital-of-philadelphia) and the University of Pennsylvania before being recruited to lead the Department of Pediatrics at Brown in 2015.[1](https://www.ncbi.nlm.nih.gov/books/NBK621992/) She began her [Rhode Island](https://www.edgepedia.org/rhode-island) roles on April 15, 2015.[4](https://archive2.news.brown.edu/2007-2015/articles/2014/10/dennery.html) At the time of that recruitment, her research on regulation of lung gene expression in oxidative stress, particularly the enzyme heme oxygenase, had been continuously NIH-funded for 24 years.[4](https://archive2.news.brown.edu/2007-2015/articles/2014/10/dennery.html)
## Research and contributions
Her research focuses on oxidative stress-mediated neonatal lung gene regulation and on hyperoxic lung injury and repair, with clinical interests in neonatal jaundice, BPD, and the long-term consequences of prematurity.[6](https://www.brownhealth.org/providers/phyllis-dennery-md) Bronchopulmonary dysplasia is a chronic lung disease of premature infants caused in part by the oxygen and ventilatory support needed to keep them alive; it is characterized by alveolar dysplasia and impaired vascularization.[2](https://vivo.brown.edu/display/pdennery) • [7](https://doi.org/10.1186/s12931-022-02263-8)
A central thread of her work is cellular senescence, the state in which cells stop dividing and secrete inflammatory factors. Her lab discovered that macrophage senescence is a hallmark of BPD in an animal model and defined the developmental regulation of senescence in the neonatal lung.[2](https://vivo.brown.edu/display/pdennery) The 2023 [Nature Communications](https://www.edgepedia.org/nature-communications) study established that in mice, lung senescence occurs at birth and decreases through the saccular stage; removing senescent cells at that stage disrupts lung development. In newborn mice exposed to hyperoxia, senescence increased particularly in type II cells and [secondary crest myofibroblasts](https://www.edgepedia.org/secondary-crest-myofibroblast), peaked during the alveolar stage, and was mediated by the p53/p21 pathway; clearing senescent cells during the alveolar stage attenuated hyperoxia-induced alveolar and vascular simplification. The authors concluded that early programmed senescence orchestrates postnatal lung development, whereas later hyperoxia-induced senescence causes injury through different mechanisms, defining an optimal therapeutic window for inhibiting injury-related senescence.[5](https://doi.org/10.1038/s41467-023-35985-4)
The lab's more recent work evaluates how senescence and mitochondrial bioenergetics mediate responses to oxidative stress in the hyperoxia-exposed neonatal lung, seeking interventions that mitigate injury-related senescence while preserving developmental senescence.[2](https://vivo.brown.edu/display/pdennery)
## Key publications
**Timing and cell specificity of senescence drives postnatal lung development and injury** (Nature Communications, 2023). This paper showed that senescence is required for normal postnatal lung development in mice but that hyperoxia induces a second, harmful wave of senescence in type II cells and myofibroblasts through p53/p21, and that clearing senescent cells in the alveolar stage reduces injury.
**Metabolic dysregulation in bronchopulmonary dysplasia** (Redox Biology, 2021). A review laying out metabolic dysregulation as a framework for identifying biomarkers and therapeutic approaches in BPD.[8](https://doi.org/10.1016/j.redox.2021.102104)
**Single-cell transcriptomics reveals lasting changes in the lung cellular landscape into adulthood after neonatal hyperoxic exposure** (Redox Biology, 2021). Used single-cell RNA sequencing to trace persistent alterations in lung cell populations after neonatal hyperoxia.[9](https://doi.org/10.1016/j.redox.2021.102091)
**Upregulating carnitine palmitoyltransferase 1 attenuates hyperoxia-induced endothelial cell dysfunction and persistent lung injury** (Respiratory Research, 2022). Building on the finding that endothelial Cpt1a is reduced by hyperoxia and that endothelial-specific Cpt1a knockout mice are more susceptible to injury, this study tested whether upregulating Cpt1a with baicalin or L-carnitine ameliorates hyperoxia-induced endothelial dysfunction and persistent lung injury in newborn mice.[10](https://doi.org/10.1186/s12931-022-02135-1)
**Involvement of miRNA-34a regulated Krüppel-like factor 4 expression in hyperoxia-induced senescence in lung epithelial cells** (Respiratory Research, 2022). Showed, using cultured lung epithelial cells exposed to 95% O₂, hyperoxia-exposed newborn mice, and lung samples from ventilated premature infants, that miR-34a contributes to hyperoxia-induced senescence through regulation of Krüppel-like factor 4.[7](https://doi.org/10.1186/s12931-022-02263-8)
**Identification of Heme Oxygenase-1 as a Putative DNA-Binding Protein** (Antioxidants, 2022). Combined HO-1 ChIP-seq and structural modeling to identify three probable DNA binding domains on HO-1, and showed that mutating four conserved amino acids in domain 1 altered expression of target genes, supporting a direct gene-regulatory role for HO-1.[11](https://doi.org/10.3390/antiox11112135)
**Hyperoxia impairs intraflagellar transport and causes dysregulated metabolism with resultant decreased cilia length** (AJP-Lung, 2023). Showed time-dependent cilia shortening in human airway epithelial cells after hyperoxia, with decreased abundance of intraflagellar transport proteins including dynein motors, and reduced acetylated α-tubulin in neonatal mice.[12](https://doi.org/10.1152/ajplung.00522.2021)
A companion Physiological Reports paper from 2021 showed that hyperoxia causes senescence and increases glycolysis in cultured lung epithelial cells.[13](https://doi.org/10.14814/phy2.14839)
## Honours and recognition
Dennery was elected to the National Academy of Medicine in 2014, to the Association of American Physicians in 2015, as a fellow of the Society for Free Radicals in Biology and Medicine in 2014, and as a fellow of the [American Thoracic Society](https://www.edgepedia.org/american-thoracic-society) in 2022.[2](https://vivo.brown.edu/display/pdennery) She is also a member of the American Society for Clinical Investigation; the National Academies describe these elections as among the top honors in medicine.[1](https://www.ncbi.nlm.nih.gov/books/NBK621992/) She received the Mentor of the Year award from the Eastern Society for Pediatric Research.[1](https://www.ncbi.nlm.nih.gov/books/NBK621992/)
## Leadership and service
Dennery has led the International Pediatric Research Foundation, the Society for Pediatric Research, the International Perinatal Collegium, and the Society for Redox Biology.[1](https://www.ncbi.nlm.nih.gov/books/NBK621992/) She serves on the national board of the [March of Dimes](https://www.edgepedia.org/march-of-dimes) and is Executive Committee chair for an NIH-funded pediatric clinical trials network.[2](https://vivo.brown.edu/display/pdennery) She is steering committee chair for several multi-center NHLBI-funded grants, data and safety monitoring board chair for a multi-site NHLBI study, and served on the National Academy of Medicine committee that produced the 2013 CTSA Program report.[1](https://www.ncbi.nlm.nih.gov/books/NBK621992/) She served as co-chair of the National Academies committee on Strategies to Enhance NIH-Funded Pediatric Health Research from 2024 to 2025.[3](https://www.nationalacademies.org/projects/HMD-HCS-24-07/download-bios)
## The vascular-metabolic view versus the classic model of BPD
The classic description of BPD centers on arrested alveolar development: premature lungs exposed to oxygen and ventilation develop alveolar dysplasia and impaired vascularization.[7](https://doi.org/10.1186/s12931-022-02263-8) Dennery's group frames the disease around what happens upstream of that architecture: endothelial cell dysfunction and metabolic failure. Their vascular-hypothesis work showed that hyperoxia reduces endothelial Cpt1a, that mice lacking endothelial Cpt1a are more susceptible to hyperoxia-induced injury, and that restoring Cpt1a activity protects endothelial cells and lungs, implicating fatty-acid oxidation capacity as a driver of disease.[10](https://doi.org/10.1186/s12931-022-02135-1) The 2021 Redox Biology review argues that metabolic dysregulation spans the disease and could yield biomarkers and therapies, and their glycolysis and single-cell findings tie senescence to lasting shifts in lung cell metabolism and composition.[8](https://doi.org/10.1016/j.redox.2021.102104) • [9](https://doi.org/10.1016/j.redox.2021.102091) • [13](https://doi.org/10.14814/phy2.14839)
## References
1. [Biographical Sketches of Committee Members — Strategies to Enhance NIH-Funded Pediatric Research (NCBI Bookshelf)](https://www.ncbi.nlm.nih.gov/books/NBK621992/)
2. [Dennery, Phyllis — Brown University VIVO research profile](https://vivo.brown.edu/display/pdennery)
3. [Strategies to Enhance Pediatric Health Research — Committee biographies (National Academies)](https://www.nationalacademies.org/projects/HMD-HCS-24-07/download-bios)
4. [Dennery to lead pediatrics at Lifespan, Brown — News from Brown](https://archive2.news.brown.edu/2007-2015/articles/2014/10/dennery.html)
5. [Timing and cell specificity of senescence drives postnatal lung development and injury, Nature Communications (2023)](https://doi.org/10.1038/s41467-023-35985-4)
6. [Phyllis Dennery, MD — Brown University Health](https://www.brownhealth.org/providers/phyllis-dennery-md)
7. [Involvement of miRNA-34a regulated Krüppel-like factor 4 expression in hyperoxia-induced senescence, Respiratory Research (2022)](https://doi.org/10.1186/s12931-022-02263-8)
8. [Metabolic dysregulation in bronchopulmonary dysplasia, Redox Biology (2021)](https://doi.org/10.1016/j.redox.2021.102104)
9. [Single-cell transcriptomics reveals lasting changes in the lung cellular landscape into adulthood after neonatal hyperoxic exposure, Redox Biology (2021)](https://doi.org/10.1016/j.redox.2021.102091)
10. [Upregulating carnitine palmitoyltransferase 1 attenuates hyperoxia-induced endothelial cell dysfunction and persistent lung injury, Respiratory Research (2022)](https://doi.org/10.1186/s12931-022-02135-1)
11. [Identification of Heme Oxygenase-1 as a Putative DNA-Binding Protein, Antioxidants (2022)](https://doi.org/10.3390/antiox11112135)
12. [Hyperoxia impairs intraflagellar transport and causes dysregulated metabolism with resultant decreased cilia length, AJP-Lung (2023)](https://doi.org/10.1152/ajplung.00522.2021)
13. [Hyperoxia causes senescence and increases glycolysis in cultured lung epithelial cells, Physiological Reports (2021)](https://doi.org/10.14814/phy2.14839)
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*Topic: Encyclopedia › Life and health › Life and health scientists › Life scientists › Researchers in molecular and cell biology › Molecular biology of the cell / cell signaling › Stress and developmental signaling researchers › Stress, hypoxia, and metabolism researchers*
*Initially written Sep 17, 2026 · Reviewed: Sep 30, 2026 · Edited: Sep 30, 2026; Oct 11, 2026; Oct 15, 2026; Oct 21, 2026 · Last review: Sep 30, 2026*
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License: Edgepedia Community License 1.0, https://www.edgepedia.org/edgepedia/license