PhD Scientific Days 2026
Budapest, 16-18 June 2026
Theoretical and Translational Medicine 1.
Sigma-1 Receptor as a Novel Therapeutic Target in Diabetic Kidney Disease
Előadó neve
Ms. Kállay, Hanga
Neptune code
JF6LOM
Előadó munkahelye
Semmelweis University, Pediatric Center
Előadó telefonszáma
06205349409
Előadó e-mail címe
kallayhanga@gmail.com
Az előadás címe
Sigma-1 Receptor as a Novel Therapeutic Target in Diabetic Kidney Disease
Szerző(k) neve és munkahelye
Hanga Kallay1,2, Akos Toth1,2, Dora B. Balogh1, Marcell Cserhalmi1, Alexandra Rozsahegyi1,2, Lilla Lenart1,2, Judit Hodrea1,2, Attila J. Szabo2, Adam Hosszu1,2, Andrea Fekete1,2
1: MTA-SE „Lendület” Momentum Diabetes Research Group, Budapest, Hungary
2: Pediatric Center, Semmelweis University, Budapest, Hungary
Bemutatás módja
Szóbeli
Szekció
Theoretical and Translational Medicine 1.
Language of the presentation
English
Preferred session
Theoretical and Translational Medicine
Összefoglaló szövege
Introduction: Diabetic kidney disease (DKD) is the leading cause of chronic kidney disease. Current treatments cannot halt the progression of renal injury, highlighting an urgent need for therapies targeting key disease mechanisms. Previously, we described the protective role of Sigma-1 receptor (S1R) agonist fluvoxamine (FLU) in acute kidney injury. Thus, we hypothesized a similar protective effect in DKD.
Aims: We designed this study to explore the potential renoprotective benefits of S1R activation in DKD.
Method: Diabetes mellitus was induced in male Wistar rats using streptozotocin, followed by a seven-week FLU treatment. Metabolic and renal parameters were assessed along with a histological analysis of glomerular damage (PAS) and tubulointerstitial fibrosis (Masson’s trichrome). The effects of inflammation and hypoxia were tested in lipopolysaccharide (LPS)- or hypoxia-induced human proximal tubular cells (HK-2). Cells were treated with FLU. Inflammatory and hypoxia markers were measured by RT-qPCR.
Results: FLU improved renal function and urinary biomarkers of tubular damage (KIM-1, NGAL) in DKD rats. In parallel, FLU reduced glomerular damage and fibrosis. FLU decreased LPS-induced TLR2, NFKB1, and IL6 expressions, as well as hypoxia-induced HIF1A, SLC2A1, VEGFA, and TGFB1 elevation in HK-2 cells.
Conclusion: S1R activation can slow DKD progression by modulating critical inflammatory, hypoxic, and fibrotic pathways. Thus, S1R may serve as a promising novel therapeutic target in DKD.
Funding: LP2021-3/2021, TKP2021-EGA-24, 2024-1.2.3-HU-RIZONT-2024-00056
University
Semmelweis University
Supervisor
Prof. Andrea Fekete, Dr. Adam Hosszu
Publication of my abstract
I give consent to the publication of my abstract on the website of the congress.
phd.section.field
before finishing undergraduate studies (TDK, MD-PhD)
Kind
Szabad
Status
elfogadva
Accepted presentation method
szóbeli
Előadás fájl jóváhagyás
jóváhagyta
Előadó
9812
Start
10:00
End
10:10