Finding My Research Direction: A Young Palestinian Pharmacologist’s Journey to a PhD.
I am originally a refugee from Jerusalem, now living in Jericho in the West Bank. Living conditions for Palestinians in the West Bank are severely constrained by military occupation, movement restrictions, settlement expansion, and limited access to resources and economic opportunities.1,2 I began my career as a pharmacist in the West Bank, a role that carried not only the responsibility of caring for vulnerable patients, but also the personal burden of going through military checkpoints daily because of restricted freedom of movement. Even now, travelling between Nottingham and home requires complex journeys through Jordan’s airport. Following highly restricted and uncertain border crossing times to the West Bank made visits to family logistically and emotionally demanding. Facing these challenges continues to strengthen my resilience, sense of responsibility, and determination to contribute meaningfully to alleviating the suffering of others.
Palestinian pharmaceutical companies depend on imported active ingredients to manufacture dosage forms for sale in the market, leaving little space for innovation, preclinical research, or early-stage drug discovery. Recognizing this gap highlighted for me the critical need for establishing independent pharmacological research in my home country. It was during my work as a pharmacist that my interest in molecular pharmacology began, driven by my desire to contribute to scientific development and improved healthcare outcomes. At that time, I was honored to have been awarded the prestigious Chevening Scholarship by the British Foreign, Commonwealth and Development Office enabling me to pursue a Master of Science in Drug Discovery at the University of Nottingham. Through this degree, I was introduced in greater detail to molecular pharmacology, particularly through the strong and innovative research being conducted in this area at Nottingham.
I was fortunate to complete my Master’s research project under the supervision of Professor Stephen J. Hill and Dr Laura Kilpatrick in the Cell Signalling Research Group, focusing on G protein-coupled receptors (GPCRs). Specifically, my work examined the Mas-related G protein-coupled receptor, member D (MrgD), as part of the renin–angiotensin system (RAS), and its potential involvement in protective cardiovascular effects that counteract vasoconstriction, hypertension, cardiomyocyte hypertrophy, and myocyte fibrosis.3–6 I gained extensive laboratory experience, working with a variety of techniques including cell culture, transfection, luminescence ligand binding and internalization assays, functional cell assays, and molecular biology methods. I truly felt I belonged in the lab. I enjoyed every aspect of working at the bench, collaborating with a team, and continually learning new skills and knowledge.
After finishing my Master’s research project, I volunteered in Professor Hill's lab, even without compensation. This experience was a mere request for skills and knowledge; however, it grew to be much more. I got the chance to immerse myself in a unique, stimulating, vibrant research community that allowed me to learn and grow professionally. I learned from this experience that we should not wait for the right opportunity to reach our dream; we should create our path by seizing every possible moment, even if it is modest. Alongside the scientific training, I also found ways to share my culture with the group, including bringing traditional Palestinian sweets and dates from my hometown, which quickly became favourites in the Cell Signalling Research Group.
During that time, I found myself increasingly drawn towards pursuing a PhD and was beginning to see myself as an independent researcher. My interests were shifting further towards GPCRs, particularly their roles in inflammatory mechanisms and their broad regulatory effects on the vasculature and the development of cardiopulmonary diseases. It was at this point that I decided to pursue a PhD focusing on adenosine receptors and their involvement in inflammation.7–9 With funding from the Wellcome Trust DTP in Drug Discovery and Team Science supported by the University of Nottingham’s School of Life Sciences, I chose to continue my research journey in Nottingham because of its strong collaborative team science environment and translational focus on drug discovery.
I started my PhD in molecular pharmacology in 2024, primarily supervised by Professor Jeanette Woolard also in the Cell Signalling Research Group at Nottingham. My research focuses on the adenosine receptor subtypes A2A and A2B, which play critical roles in a wide range of physiological processes, including cardiovascular regulation, inflammation, metabolism, and immune responses.10–13 Therefore, understanding how these immunomodulatory checkpoints exert either protective or detrimental effects on inflammatory processes and vascular remodelling may support the development of new therapeutic strategies for cardiopulmonary diseases with inflammatory molecular pathophysiology.
I began studying A2A and A2B receptors and investigating their involvement in disease development with the plan to examine their endogenous expression levels and responses to different triggers in living cells by finding the tools that provide high spatial and temporal imaging resolution.14,15 The currently available fluorescently labelled ligands have poor photophysical properties, which restrict their use in advanced imaging applications. To address this limitation, my research aims to develop new ligands incorporating improved fluorophores offering greater brightness, photostability, and flexibility.
The ability to develop such tools could allow for many applications, ranging from studying receptor localisation to receptor trafficking, internalisation, and signalling kinetics in living systems ultimately at endogenous receptor expression levels. This would provide the opportunity to visualise adenosine receptor distribution and signalling in cardiopulmonary tissues and to investigate how these pathways are altered during inflammation, hypoxia, and vascular remodelling. In turn, this may support the development of novel therapeutics for cardiopulmonary and inflammatory diseases.
Looking ahead, my PhD is not only a continuation of my scientific training, but also a way to engage in research that addresses diseases with complex inflammatory and vascular components, given that cardiopulmonary diseases remain a major health burden. Through my work on adenosine receptor signalling and the development of improved tools to study these pathways, I hope to contribute to a better understanding of their role in disease and, in the longer term, to support the development of more effective therapeutic approaches. Ultimately, I aim to use the skills and experience gained during my PhD to continue building a research career that makes a meaningful impact in pharmacology and helps improve patient outcomes, particularly in regions of the world most affected by healthcare disparities.
1. United Nations Office for the Coordination of Humanitarian Affairs (OCHA). Humanitarian Needs Overview: Occupied Palestinian Territory. 2023. Accessed January 26, 2026. www.ochaopt.org/content/humanitarian-needs-overview-2023
2. World Bank. Racing Against Time: World Bank Economic Monitoring Report to the Ad Hoc Liaison Committee. 2023. Accessed January 26, 2026. documents.worldbank.org/en/publication/documents-reports/documentdetail/099638209132320721
3. Jesus ICG, Mesquita T, Souza Santos RA, Guatimosim S. An overview of alamadine/MrgD signaling and its role in cardiomyocytes. Am J Physiol Cell Physiol. 2023;324(3):C606-C613. doi:10.1152/AJPCELL.00399.2021
4. Schleifenbaum J. Alamandine and its receptor mrgd pair up to join the protective arm of the renin-angiotensin system. Front Med (Lausanne). 2019;6:452260. doi:10.3389/FMED.2019.00107/BIBTEX
5. De Souza-Neto FP, De Morais E Silva M, De Carvalho Santuchi M, et al. Alamandine attenuates arterial remodelling induced by transverse aortic constriction in mice. Clin Sci. 2019;133(5):629-643. doi:10.1042/CS20180547
6. Habiyakare B, Alsaadon H, Mathai ML, Hayes A, Zulli A. Reduction of angiotensin A and alamandine vasoactivity in the rabbit model of atherogenesis: differential effects of alamandine and Ang(1-7). Int J Exp Pathol. 2014;95(4):290-295. doi:10.1111/IEP.12087
7. Haskó G, Linden J, Cronstein B, Pacher P. Adenosine receptors: therapeutic aspects for inflammatory and immune diseases. Nat Rev Drug Discov. 2008;7(9):759-770. doi:10.1038/NRD2638
8. Haskó G, Cronstein BN. Adenosine: An endogenous regulator of innate immunity. Trends Immunol. 2004;25(1):33-39. doi:10.1016/j.it.2003.11.003
9. Borea PA, Gessi S, Merighi S, Vincenzi F, Varani K. Pharmacology of Adenosine Receptors: The State of the Art. Physiol Rev. 2018;98(3):1591-1625. doi:10.1152/PHYSREV.00049.2017
10. Cai Z, Tu L, Guignabert C, Merkus D, Zhou Z. Purinergic dysfunction in pulmonary arterial hypertension. J Am Heart Assoc. 2020;9(18):17404. doi:10.1161/JAHA.120.017404/ASSET/ADDD8BA7-3972-4699-AEEE-67AF47184208/ASSETS/GRAPHIC/JAH35488-FIG-0003.PNG
11. Della Latta V, Cabiati M, Rocchiccioli S, Del Ry S, Morales MA. The role of the adenosinergic system in lung fibrosis. Pharmacol Res. 2013;76:182-189. doi:10.1016/J.PHRS.2013.08.004
12. Sparks H V., Bardenheuer H. Regulation of adenosine formation by the heart. Circ Res. 1986;58(2):193-201. doi:10.1161/01.RES.58.2.193
13. Newby AC, Worku Y, Holmquist CA. Adenosine formation. Evidence for a direct biochemical link with energy metabolism. Adv Myocardiol. 1985;6:273-284. Accessed October 6, 2024. europepmc.org/article/MED/2986260
14. Patera F, Mistry SJ, Kindon ND, et al. A novel and selective fluorescent ligand for the study of adenosine A2B receptors. Pharmacol Res Perspect. 2024;12(4). doi:10.1002/PRP2.1223
15. Comeo E, Kindon ND, Soave M, et al. Subtype-Selective Fluorescent Ligands as Pharmacological Research Tools for the Human Adenosine A2A Receptor. J Med Chem. 2020;63(5):2656-2672. doi:10.1021/ACS.JMEDCHEM.9B01856
