PhD Scientific Days 2024

Poster Session P - Conservative Medicine

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

Előadó neve

Ms. Zrufkó, Réka

Neptun code

I3YH69

Előadó munkahelye

Semmelweis University

Előadó telefonszáma

06209803820

Előadó e-mail címe

zrufkoreka@gmail.com

Az előadás címe

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

Szerző(k) neve és munkahelye

Réka Zrufkó¹

1: Semmelweis University

Bemutatás módja

Poszter

Szekció

Poster Session P - Conservative Medicine

Language of the presentation

Hungarian

Preferred session

Conservative Medicine

Összefoglaló szövege

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

University

Semmelweis University

Supervisor

Dr. Papp Domonkos

Publication of my abstract

I give consent to the publication of my abstract on the website of the congress.

Kind

Szabad

Status

elfogadva

Accepted presentation method

poszter

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

8114

Start

16:30

End

16:33