Dr. Rafikova has received her MD and Ph.D. in Physiology at Moscow State University, the leading University of Russia. Since 2000, she worked at well-recognized universities of USA (New York University, Department of Biochemistry (2000-06), Pittsburgh University, Center for Clinical Pharmacology (2006-08), Augusta University Vascular Biology Center (2008-15). During these years, she had received extensive training in the area of cardiovascular and pulmonary diseases. From 2015 Dr. Rafikova is an Assistant Professor at the Department of Medicine, University of Arizona and leading a multidisciplinary research group and study pulmonary and cardiovascular diseases. A combination of translational and gender-oriented research makes her lab one of only a very few such academic research labs in the USA.
Dr. Rafikova’s research goal is to establish gender-specific therapeutic approaches in pulmonary arterial hypertension (PAH), a deadly disease with no effective therapy.
In particular, her current research effort is focused on the evaluation of the role of mitochondrial dysfunction and metabolic reprogramming in PAH. She has discovered that chronic inhibition of mitochondrial electron transport chain plays a causative role in PAH pathogenesis. By reproducing the human mutation in the protein responsible for mitochondrial homeostasis, she has recently developed a humanized rat model of PAH. This model is fully unique not only because it reproduced a human mutation that increases the probability to develop PAH from 10-15 cases per million to 70% of cases, but also because it is the only currently available animal model that fully reproduces the gender disparity seen in PAH patients (female to male ratio of 4:1).
Dr. Rafikova is also investigating the gender-specific regulation of redox homeostasis, which, in turn, mediates the activity of “alarmin” proteins (such as HMGB1) and contributes to manifestation of PAH. By using a combination of multiple animal models and patient samples obtained from healthy control subjects, patient with non-PAH lung or heart diseases, and PAH patient cohort her research team investigates 1) whether PAH mediates a the gender-specific changes in the redox profile that could be used as a biomarker or prognostic factor; 2) gender-specific circulating markers of “pro-inflammatory” or “proliferative” phenotype of PAH that could be used to adjust the patient therapy; 3) parameters that could serve as a blueprint of an early stage of pulmonary hypertension in order to improve diagnosis and survival rate of PAH; 4) the particular gender-specific mechanisms responsible for manifestation of PAH.
Dr. Rafikova dedicates a lot of her effort to design and test a unique peptide-based therapeutics that in contrast to the classical “small molecule” inhibitors specifically attenuate the pathological, disease driven, signaling without affecting the normal physiological function of the protein. She has four active patent applications aimed to treat different cardiovascular diseases and has submitted a Provisional Patent Application at the University of Arizona, which suggests novel gender-specific therapeutics for PAH. Other recently designed peptides that prevent the transition of pulmonary vascular cells into the highly proliferative “cancer-like” cells are currently under investigation.