Md Khadem Ali
Dr. Ali joined Juvena Therapeutics as a Pharmacology Scientist to lead the in vivo studies for the adipose and pulmonary research programs. He is an accomplished lung biologist with 10 years of a strong background in inflammatory, allergic, respiratory, pulmonary vascular, and infectious diseases. His overarching goal is to discover improved therapies for individuals with lung and metabolic diseases.
Dr. Ali’s academic training and research experience across 4 nations and 3 continents have provided him with an excellent background in multiple biological disciplines, including immunology, molecular biology, microbiology, and cell biology. He received a B. Sc in Biotechnology and Genetic Engineering from Khulna University, Bangladesh, an M.Sc. in Systems Biotechnology from Chung-Ang University, South Korea, and a Ph.D. in Immunology and Microbiology from the University of Newcastle, Australia. His Ph.D. focused on investigating how iron, infection, and immunity affect one another in the context of lung diseases, including asthma, COPD, and IPF. These studies showed that increased iron in the lung is associated with small airway fibrosis, inflammation, and reduced lung function in systemic iron-overloaded mouse models. Targeting with an iron chelator drug prevented airway fibrosis and lung function reduction in a mouse model of IPF, highlighting the potential for a novel therapeutic approach to this disease. Having shown iron overload in clinical asthma, he used two mouse models of systemic iron overload and showed that this was associated with inflammation, increased mucus secretion, and scarring in the airways. Subsequent studies demonstrated that the combined treatment with the iron chelator deferoxamine and antibiotic tobramycin reversed lung dysfunction in mice infected with Pseudomonas aeruginosa. As a postdoctoral fellow at Stanford, he investigated ways to enhance bone morphogenic protein 2 (BMPR2), a gene that is haploinsufficient or reduced in expression and function in PAH, a disease of lung blood vessel dysfunction. RNAseq, siRNA-mediated high throughput screening, and in vitro and in vivo models led to the identification of two proteins, PTP1b and ELK3 as modifiers of BMPR2 signaling. In addition, his research discovered two long non-coding RNAs LINC02593 and RGMB-AS1, that modulate BMPR2 signaling and pulmonary vascular remodeling. A second project focused on hemorrhagic telangiectasia (HHT), a related disease associated with mutations in ALK1, ENG, and SMAD4. He identified a small molecule drug that activates BMPR2 signaling and inhibits VEGF signaling pathways, two critical pathways in HHT.
To date, he has published 36 peer-reviewed high-impact publications, 12 as first author and 9 as a second author (average IF >10, with 800+ citations), 23 conference abstracts, 13 conference presentations, 2 book chapters, 1 patent, and 2 funded research grants. His research was also selected for oral and poster presentations at international/national conferences. Recognizing his contributions, he received seven academic and research awards. He mentored 5 undergraduates, 1 junior Ph.D. student, demonstrated immunology and microbiology lab course for 3 years, and 1 high school summer student. He took on a leadership role as a co-Director of the Stanford Cardiovascular Institute Postdoc conference 2020. In addition, he has been regularly invited to conduct peer reviews for elite journals in the pulmonary medicine field.
Beyond academic, professional life, he enjoys traveling, playing, and watching cricket, watching movies.
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