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Priti Azad, Ph.D.

priti azad

​My research goal is to understand the genetic basis of adaptations using both in-vivo as well as in-vitro model systems which can be translated in future towards therapies for human. I have used various model systems (Drosophila, Human in-vitro cells) to study hypoxia tolerance under different paradigms-chronic, acute, intermittent and constant hypoxia. Furthermore, my continuous interest in stem cells has motivated me to build a human iPS cells derived erythroid model system to study hypoxia induced polycythemia from Andean population that have been adapted to low oxygen for thousands of generations. Interestingly, in that Andean region (Cerro de pasco) resides 2 populations: one that is adapted and have near normal hematocrit levels and one that is mal-adapted and show an exaggerated response in terms of RBCs production and suffer from Monge’s disease (Chronic Mountain Sickness-CMS). Intriguingly women in the region are protected at high altitude through estrogen which mediates the excessive RBC production response until menopause! By successfully replicating the “excessive erythropoietic response in the dish” of the CMS patients and the lack-thereof of the non-CMS adapted subjects, I now aim on studying various aspects of mechanism(s) (genetic, epigenetics, non-coding RNA, hormonal and inhibitors - as shown in my collaborations) that regulate erythropoiesis in this population with the help of great collaborations within and outside of UCSD. 


  1. Azad P, Villafuerte FC, Bermudez D, Patel G, Haddad GG. 2021. Protective role of estrogen against excessive erythrocytosis in Monge's disease. Exp Mol Med 53: 125-135.
  2. Zhao H, Azad P, Yao H, Wu W, Dwivedi I, Haddad GG. 2021. IPSCs Technology to Model Chronic Mountain Sickness. In Elsevier Series: Current Progress in iPSC Disease Modeling (pp.45-63).
  3. Zhou D, Azad P, Stobdan T, Haddad GG. 2021. Mechanisms Regulating Hypoxia Tolerance in Drosophila and Humans. In book: Stress: Genetics, Epigenetics and Genomics (pp.241-251).
  4. Bermudez D, Azad P, Figueroa-Mujica R, Vizcardo-Galindo G, Corante N, Guerra-Giraldez C, Haddad GG, Villafuerte FC. 2020. Increased hypoxic proliferative response and gene expression in erythroid progenitor cells of Andean highlanders with chronic mountain sickness. Am J Physiol Regul Integr Comp Physiol 318: R49-R56.
  5. Azad P, Stobdan T, Zhou D, Hartley I, Akbari A, Bafna V, Haddad GG. 2017. High-altitude adaptation in humans: from genomics to integrative physiology. J Mol Med 95: 1269-1282.
  6. Stobdan T, Akbari A, Azad P, Zhou D, Poulsen O, Appenzeller O, Gonzales GF, Telenti A, Wong EHM, Saini S et al. 2017. New Insights into the Genetic Basis of Monge's Disease and Adaptation to High-Altitude. Mol Biol Evol 34: 3154-3168.
  7. Azad P, Zhao HW, Cabrales PJ, Ronen R, Zhou D, Poulsen O, Appenzeller O, Hsiao YH, Bafna V, Haddad GG. 2016. Senp1 drives hypoxia-induced polycythemia via GATA1 and Bcl-xL in subjects with Monge's disease. J Exp Med 213: 2729-2744.
  8. Yao H, Azad P, Zhao H, Wang J, Poulsen, O, Freitas, BC, Muotri, AR, Haddad, GG. 2016. Ha The Na+/HCO3- co-transporter is protective during ischemia in astrocytes. Neuroscience. 2016 Dec 17;339:329-337.
  9. Azad P, Zhou D, Zarndt R, Haddad GG. 2012. Identification of Genes Underlying Hypoxia Tolerance in Drosophila by a P-element Screen. G3 (Bethesda). 2012 Oct; 2(10):1169-78.
  10. Azad P, Zhou D, Russo E, Haddad GG. 2009. Distinct Mechanisms Underlying Tolerance to Intermittent and Constant Hypoxia in Drosophila melanogaster. PLoS ONE 4(4): e5371.