PhD Scientific Days 2024

Poster Session P - Conservative Medicine

The role of PARK7 in ischemia-reperfusion induced acute renal failure

Text of the abstract

The role of PARK7 in ischemia-reperfusion induced acute renal failure

Réka Zrufkó1, Beáta Szebeni1,2, Apor Veres-Székely1,2, Csenge Pajtók1, Péter Bokrossy1, Csenge Szász1, Attila J. Szabó 1,2, Ádám Vannay 1,2, Domonkos Pap1,2
1 Pediatric Center, MTA Center of Excellence, Semmelweis University, 1083 Budapest, Hungary
2 HUN-REN–SU Pediatrics and Nephrology Research Group, 1052 Budapest, Hungary

Aims: Acute renal failure (ARF) has a high risk of morbidity and mortality without reliable therapeutic intervention. The most common cause of ARF is renal ischemia reperfusion (I/R) injury which may associated with various clinical situations including sepsis, cardiac arrest or organ transplantation. Our aim was to better understand the renal I/R injury associated proteomic changes to find new therapeutic targets.
Methods: Proteomic evaluation was carried out on kidneys of rats following I/R injury. The significantly changed proteins were analyzed by bioinformatics approaches. The in vitro effect of Parkinson’s diseases 7 (PARK7) on oxidative stress (H2O2) induced cell death was investigated by its pharmacological activation on kidney epithelial cells (HEK-293 and HK-2). Effect of pharmacological activation of PARK7 was determined in I/R and lipopolysaccharide (LPS) induced mice models of ARF.
Results: PARK7 was identified as central factor related to I/R induced oxidative stress of the kidney. Pharmacological activation of PARK7 decreased H2O2 induced death of HEK-293 and HK-2 cells. Accordingly, pharmacological activation of PARK7 improved renal function in mice following I/R and LPS induced ARF.
Conclusion: Our data suggest that PARK7 plays a role in the reduction of renal I/R injury associated oxidative damage probably through activation of antioxidant or anti-apoptotic mechanisms. Therefore, PARK7 may serve as therapeutic target in the treatment of I/R injury induced ARF.

Grant: K-142728, TKP2021-EGA-24, ELKH-POC-2022-024, ÚNKP-23-3-I-SE-36, ÚNKP-23-3-I-SE-42, ÚNKP-23-4-II-SE-29, ÚNKP-23-5-SE-15; Hungarian Academy of Sciences, János Bolyai Research Scholarship.


Réka Zrufkó
zrufkoreka@gmail.com / zrufko.reka@phd.semmelweis.hu

Semmelweis University
Károly Rácz conservative medicine division - Doctoral School of Clinical Medicine

Supervisor: Dr. Papp Domonkos