Trainee Spotlight: Hyunyun Kim’s Research Project Wins Top Honors in 2023 CST Research Training Award

Congratulations to Hyunyun Kim for his selection as one of the top three recipients for the 2023 CST Research Training Award for his research project, “Importance of microvascular stress pathways in renal dysfunction caused by ischemi-reperfusion injury: role of apoptosis, necroptosis, and autophagy” from the Canadian Society of Transplantation (CST)! Hyunyun is a Ph.D. student at the Université de Montréal, under the supervision of Dr. Marie-Josée Hébert. His research interests are centered around the mechanisms of cell death and autophagy in acute kidney injury induced by ischemia-reperfusion injury. This is a well-deserved recognition of Hyunyun’s hard work and dedication to advancing their field of study.

This year the CST Awards ceremony (October 19, 2023) will be held live during the 2023 CST Annual Scientific Meeting (October 16-20, 2023). Congrats again to Hyunyun for this achievement!

About Hyunyun Kim

Hyunyun Kim is a Ph.D. student at the Université de Montréal. He completed a Bachelor’s of Science at Yeungnam University and a Master’s of Science degree at Pusan National University in South Korea. After completing his Master’s degree, he pursued his research activity at the medical research center of the Pusan National University Hospital (PNUH) and the Yeungnam University Medical Center (YUMC) as a research assistant. He then joined Dr. Hébert’s lab in 2019. His research interests are focused on the crosstalk and mechanisms of cell death and autophagy in acute kidney injury (AKI) induced by ischemia-reperfusion injury (IRI).

Lay Abstract: Importance of microvascular stress pathways in renal dysfunction caused by ischemi-reperfusion injury: role of apoptosis, necroptosis, and autophagy

Acute kidney injury (AKI) consists of a sudden loss of kidney function. Ischemia-reperfusion is a common cause of AKI, especially after renal transplantation. AKI can lead to chronic kidney disease (CKD), a progressive and irreversible deterioration of kidney function. Therefore, understanding the mechanisms leading to the transition from AKI to CKD is important for preventing the premature loss of transplanted kidneys. We found that the death of microscopic vessels during AKI is the most important factor that predicts the irreversible loss of renal function.

We also found that AKI activates different types of stress and death responses in renal microscopic vessels and tubules over time. How these stress and death responses interact with one another to protect or injure the renal microscopic blood vessels remains to be studied. We will build on these observations to study the role and importance of autophagy, a protective stress response and two types of cell death responses, apoptosis and necroptosis, in the loss of renal function after ischemia-reperfusion injury. We also plan to identify new biomarkers that will ultimately help follow, in patients, the types of stress and death responses that are activated in transplanted kidneys.

These results will help define new ways to protect kidneys from premature loss after transplantation.