- Chronic respiratory diseases (asthma, cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD)) are a major global health burden and the fourth greatest cause of death. These patients are prone to bacterial infections particularly P. aeruginosa. My research is focused on the identification of novel virulence factors/mechanism utilized by the pathogen. This led to the discovery of “theft-ferroptosis”- where P. aeruginosa hijacks the host lipid-peroxidation machinery/cell death pathway for pathogenesis.
- H. H. Dar*, T. S. Anthonymuthu, P. A. Ponomareva et al., (2021). A new thiol- independent mechanism of epithelial host defense against Pseudomonas aeruginosa: iNOS/NO sabotage of theft-ferroptosis. Redox Biology. 45, 102045. https://doi.org/10.1016/j.redox.2021.102045 (*Co-corresponding author). (PMID: 34167028).
- H. H. Dar, Y. Y. Tyurina, K. Mikulska-Ruminska, I. Shrivastava, H.C. Ting, et al., (2018). Pseudomonas aeruginosa utilizes host polyunsaturated phosphatidylethanolamines to trigger theft-ferroptosis in bronchial epithelium. Journal of Clinical Investigation. 128 (10):4639-4653. (PMID:30198910).
- Radiation exposure/injury occurring unintentionally in catastrophic situations or because of nuclear weapons testing or potential terroristic attacks poses a significant public health risk and demands development of drugs and biologics as medical countermeasures for acute radiation syndrome (ARS). We have identified radiation induced ferroptotic cell death of gut epithelial cells as a crucial intervention target for mitigation of radiation injury/death. Part of my research is focused on development ferroptosis cell death inhibitors as new radiomitigators.
- H. H. Dar et al., (2023). Discovering selective antiferroptotic inhibitors of the 15LOX/PEBP1 complex noninterfering with biosynthesis of lipid mediators. Proc Natl Acad Sci U.S.A. 120(25): e2218896120. (PMID: 37327313).
- H. H. Dar, et al., (2022). P. aeruginosa augments irradiation injury via 15-lipoxygenase–catalyzed generation of 15-HpETE-PE and induction of theft-ferroptosis. JCI Insight;7(4): e156013. https://doi.org/10.1172/jci.insight.156013 (PMID: 35041620).
- Ferroptosis is a new field of study, discovered in 2012, which is centered on non-apoptotic form of cell death that is dependent on the connection between iron and lipid peroxidation and highly relevant in various diseases including degenerative diseases and malignancies. My goal is to exploit ferroptosis as a therapeutic intervention target and develop specific inhibitors for diseases like chronic respiratory diseases (asthma, CF, COPD, pneumonias), radiation injury and cancer.
- A. Kapralov*, Q. Yang*, H. H. Dar*, et al., (2020). Redox lipid reprogramming commands susceptibility of macrophages and microglia to ferroptotic death. Nature Chemical Biology.16:278-290.(PMID:32080625) (* Equal contribution).
- S. E. Wenzel, Y. Y. Tyurina, J. Zhao, C. M. St. Croix, H. H. Dar, et al., (2017). PEBP1 Wardens ferroptosis by enabling lipoxygenase generation of lipid death signals. Cell. 171(3):628-641. (PMID:29053969).
Education
2001 | Aligarh Muslim University, Aligarh, UP, India | BS, Chemistry
2003 | School of Biotechnology, University of Jammu, Jammu, J&K, India | MS, Biotechnology
2011 | Institute of Microbial Technology/Jawaharlal Nehru University, New Delhi, India | PhD, Biochemistry and Molecular Biology
2014 | Research Center, Hospital Maisonneuve- Rosemont (HMR), University of Montreal, Quebec, Canada. | Postdoctoral Fellow, Biochemistry and Cell Biology
2014 | McMaster University, Hamilton, Ontario, Canada | Visiting Fellow, Microbiology
