Yongneng Zhang
A CRITICAL CONTRIBUTION OF A GENETIC VARIANT IN THE TRANSITION FROM NORMAL FUNCTION TO FAILURE OF THE RIGHT HEART IN PULMONARY ARTERIAL HYPERTENSION
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Scholarship:
2023 Paroian Family PH Research Scholarship
Research group: Faculty of Medicine and Dentisty, University of Alberta
Under the supervisor: Mr. Michelakis, Professor and Vice Chair (Research)
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About Yongneng Zhang
Dr. Yongneng Zhang earned his Bachelor’s degree in Medicine and Surgery from Nanchang University, followed by an MSc from Shantou University in China. He just obtained his PhD at the University of Alberta in November 2023. Dr. Zhang is currently taking a post-doctoral fellowship under the supervision of Dr. Evangelos Michelakis, a clinician-scientist in the cardiology division at the University of Alberta.
Dr. Zhang has received numerous competitive awards for his contributions to translational research, including the Paul Man Award and the Med Star Graduate Student Award at the University of Alberta. In addition, his translational work was recognized as a finalist for the 2023 Cournand and Cooper Early Career Investigator Award of the American Heart Association.Â
Projects:
A critical contribution of a genetic variant in the transition from normal function to failure of the right heart in pulmonary arterial hypertension (2023)
Unlike hypertension, pulmonary arterial hypertension (PAH) is a disease that has increased blood pressure in the pulmonary (lung) circulation. However, even when treated with costly medications, this disease is uncurable, inducing premature deaths. The main driver of mortality in PAH is not the pulmonary blood pressure but the function of the right heart. What makes the transition from normal function to failure of the right heart in PAH is unknown. We found the transition is not due to heart muscle cell failure as thought until now. It may be determined by a specific cell type called myofibroblasts, which account for the most cell numbers in injured hearts but are very few in healthy hearts. Moreover, we showed that the activation of the myofibroblasts is related to the level of a mitochondrial protein UCP2 with a function of cellular calcium uptake. In a small cohort of patients with PHT, we found the carriers of the UCP2 gene variant have decreased right heart function compared to non-carriers that had similar pulmonary blood pressures, making this UCP2 gene variant a potential biomarker that could predict right heart failure in PHT patients if confirmed in larger cohorts.