Education

  • PhD, Semmelweis University of Budapest, 2004, Clinical Medicine (summa cum laude honors)
  • Master of Sciences, Technical University of Budapest, Hungary, 1999,  Bioengineering, Faculty of Chemical Engineering,

Research Interests

Dr. Stadler's Oxidative Stress and Disease lab is focused on redox biology, with emphasis on diabetes, insulin resistance and diabetic nephropathy (DN). The research generated from his lab focuses on the exact free radical mechanisms that can play a role in the pathogenesis of these conditions, ultimately contributing to insulin resistance or leading to tissue damage and to complications.

Currently, Dr. Stadler and his team are interested in:

  • Understanding the redox signaling roles of reactive lipids and mitochondrial lipid hydroperoxides;

  • Understanding the specific role of redox signaling in an important complication of diabetes: diabetic nephropathy. For this project we use high fat diet models, diabetic models with significant renal pathology, transgenic and pharmacological approaches and kidney cell lines studying proximal tubular cells and podocytes. Loss of podocytes - which are important cells in the integrity of the filtration barrier in the kidney - is characteristic to obesity and diabetic nephropathy. Loss of podocytes will result in proteinuria and renal complications. Treatments for hyperglycemia and high blood pressure do not stop podocyte loss, indicating that other important factors must exits. Little is known about redox signaling mechanisms and the role of reactive lipids in controlling podocyte survival and death. Identifying these mechanisms has high clinical significance as it may help designing targeted therapies to prevent diabetic nephropathy or similar proteinuric diseases.

Besides podocytes, a second project deals with proximal tubular cells and their mitochondrial metabolism. This is because a) tubular cell injury correlates best with mortality in diabetic nephropathies, b) eventually almost all kidney diseases culminate into tubulointerstitial fibrosis. New research from us and others indicate that tubular injury may also be a primary event in DN rather than just a secondary consequence. Prevention here therefore would be of high importance as well.

Through the use of in vivo electron spin resonance (EPR) methodologies Dr. Stadler and his team are able to specifically detect increased free radical production in tissues or cells. Low temperature EPR from frozen samples can be used to evaluate the integrity of various protein complexes, for example the different components of the electron transport chain. In addition, the combination of EPR and other techniques (e.g. confocal microscopy, immunohistochemistry, XF24 extracellular flux analyzer) provides an additional conceptual innovation to studies.

Research in Dr Stadler’s laboratory is currently funded by the Pennington Foundation, and through grant support by NIDDK 1R01-DK137472 (PI: Stadler).

Department: Oxidative Stress and Disease

Selected Publications

  1. Lee AH, Orliaguet L, Youm YH, Maeda R, Dlugos T, Lei Y, Coman D, Shchukina I, Andhey S, Smith SR, Ravussin E, Stadler K, Hyder F, Artyomov MN, Sugiura Y, Dixit VD. (2025) Cysteine depletion triggers adipose tissue thermogenesis and weight-loss. Nat Metab 7:1204-1222.

  2. Stadler K, Ilatovskaya DV (2023) Renal epithelial mitochondria: implications for hypertensive kidney disease. Compr Physiol 14(1):5225-5242.

  3. Wang Q, Qi H, Wu Y, Yu L, Bouchareb R, Li S, Lassen E, Casalena G, Stadler K, Ebefors K, Yi Z, Shi S, Salem F, Gordon R, Lu L, Williams RW, Duffield J, Zhang W, Itan Y, Bottinger E, Daehn IS. (2023) Genetic susceptibility to diabetic kidney disease is linked to promoter variants of XOR. Nat Metab 5(4):607-625.

  4. McCrimmon A, Corbin S, Shrestha B, Roman G, Dhungana S, Stadler K (2022) Redox phospholipidomics analysis reveals specific oxidized phospholipids and regions in the diabetic mouse kidney. Redox Biol 58:102520. doi: 10.1016/j.redox.2022.102520.

  5. McCrimmon A, Cahill KM, Kruger C, Mangelli M, Bouffard E, Dobroski T, Michanczyk KN, Burke SJ, Noland RC, Ilatovskaya DV, Stadler K (2022) Intact mitochondrial substrate efflux is essential for prevention of tubular injury in a sex-dependent manner. JCI Insight 7(7):e150696.

  6. Kruger C, Nguyen TT, Breaux C, Guillory A, Mangelli M, Fridianto KT, Kovalik JP, Burk D, Noland RC, Mynatt RL, Stadler K. (2019) Proximal tubular cell-specific ablation of carnitine acetyltransferase causes tubular disease and secondary glomerulosclerosis. Diabetes. 68(4):819-831.

NCBI Bibliography