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Mitochondria
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Research Group Mitochondrial Toxicology

Zischka Group

We focus on Mitochondrial Damage upon diverse aspects of cell-toxic conditions in human disease, e.g. metabolic diseases, neurodegeneration, cancer, organ failure.

We focus on Mitochondrial Damage upon diverse aspects of cell-toxic conditions in human disease, e.g. metabolic diseases, neurodegeneration, cancer, organ failure.

About our Research

More than one hundred publications document the research of the AG Zischka about mechanisms, molecular targets, pathognomonic consequences and potential therapies of mitochondrial impairments. Their research focus may thus be best termed as “Mitochondrial Toxicology”. Regarded over decades as simple power plants of the cell, the current apprehension of mitochondria is to be the key player of cell homeostasis and cell death. In their work, the AG Zischka has achieved major methodological breakthroughs in mitochondrial analyses, such as the separation of damaged from intact organelles – a USP of this group, or the unprecedented isolation of intact mitochondria from tumor cells or minute sample amounts such as liver biopsies.

Using a unique platform with a plethora of analytical methods and assays, the AG Zischka studies mitochondrial impairments, signaling alterations, dysregulation and damage in human disease. Foremost this implies work on metabolic diseases such as NASH or obesity, liver failure, neurodegeneration, cardiac issues and cancer. A major aim thereto is the development of strategies to either rescue/amend mitochondrial function or to cause their targeted destruction in the case of cancer.

 

The impact of the AG Zischka work may be best exemplified by their results concerning the rare but severe Wilson disease. They have unraveled the decisive role of mitochondrial impairment at major crossroads in this devastating disease (JCI 2011, NYAS 2014, Tox in vitro 2018, Gastroenterology 2018, IJBCB 2018, Gastroenterology 2019, Cell Stress 2020, J Hep 2020, Metallomics 2020, Life Sci Alliance. 2021), a still ongoing work. Based on their findings, they could come up with innovative therapeutic compounds that resulted in unprecedented therapeutic efficacy, thus allowing for a new treatment strategy that is currently in the development towards the clinics (JCI 2016, JTEMB 2018, CMGH 2019, ISMEJ 2021, Appl Environ Microbiol. 2021).

More than one hundred publications document the research of the AG Zischka about mechanisms, molecular targets, pathognomonic consequences and potential therapies of mitochondrial impairments. Their research focus may thus be best termed as “Mitochondrial Toxicology”. Regarded over decades as simple power plants of the cell, the current apprehension of mitochondria is to be the key player of cell homeostasis and cell death. In their work, the AG Zischka has achieved major methodological breakthroughs in mitochondrial analyses, such as the separation of damaged from intact organelles – a USP of this group, or the unprecedented isolation of intact mitochondria from tumor cells or minute sample amounts such as liver biopsies.

Using a unique platform with a plethora of analytical methods and assays, the AG Zischka studies mitochondrial impairments, signaling alterations, dysregulation and damage in human disease. Foremost this implies work on metabolic diseases such as NASH or obesity, liver failure, neurodegeneration, cardiac issues and cancer. A major aim thereto is the development of strategies to either rescue/amend mitochondrial function or to cause their targeted destruction in the case of cancer.

 

The impact of the AG Zischka work may be best exemplified by their results concerning the rare but severe Wilson disease. They have unraveled the decisive role of mitochondrial impairment at major crossroads in this devastating disease (JCI 2011, NYAS 2014, Tox in vitro 2018, Gastroenterology 2018, IJBCB 2018, Gastroenterology 2019, Cell Stress 2020, J Hep 2020, Metallomics 2020, Life Sci Alliance. 2021), a still ongoing work. Based on their findings, they could come up with innovative therapeutic compounds that resulted in unprecedented therapeutic efficacy, thus allowing for a new treatment strategy that is currently in the development towards the clinics (JCI 2016, JTEMB 2018, CMGH 2019, ISMEJ 2021, Appl Environ Microbiol. 2021).

Our Scientists

Prof. Dr. rer. nat. Hans Zischka

Group Leader Oxidative Cell Death

Tamara Rieder

Technical Assistant Zischka Lab

Jonas Engler

Doctoral Researcher Zischka Lab

Carola Eberhagen

Technical Assistant Zischka Lab

Dr. Adrian Jauch

Postdoc Zischka Lab

Adriana Filipa da Silva Fontes

Doctoral Researcher Zischka Lab

Dennis Koob

Doctoral Researcher Zischka Lab

Quirin Reinold

Technical Assistant Zischka Lab

Judith Sailer

Doctoral Researcher Zischka Lab

Our Publications

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2024 Scientific Article in Metabolism: clinical and experimental

Fontes, A. ; Pierson, H. ; Bierła, J.B. ; Eberhagen, C. ; Kinschel, J. ; Akdogan, B. ; Rieder, T. ; Sailer, J. ; Reinold, Q. ; Cielecka-Kuszyk, J. ; Szymanska, S. ; Neff, F. ; Steiger, K. ; Seelbach, O. ; Zibert, A. ; Schmidt, H.H. ; Hauck, S.M. ; von Toerne, C. ; Michalke, B. ; Semrau, J.D. ; DiSpirito, A.M. ; Ramalho-Santos, J. ; Kroemer, G. ; Polishchuk, R.S. ; Azul, A.M. ; DiSpirito, A. ; Socha, P. ; Lutsenko, S. ; Zischka, H.

Copper impairs the intestinal barrier integrity in Wilson disease.

2024 Scientific Article in Journal of Clinical Investigation

Tsvilovskyy, V. ; Ottenheijm, R. ; Kriebs, U. ; Schütz, A. ; Diakopoulos, K.N. ; Jha, A.N. ; Bildl, W. ; Wirth, A. ; Böck, J. ; Jaślan, D. ; Ferro, I. ; Taberner, F.J. ; Kalinina, O. ; Hildebrand, S. ; Wissenbach, U. ; Weissgerber, P. ; Vogt, D. ; Eberhagen, C. ; Mannebach, S. ; Berlin, M. ; Kuryshev, V. ; Schumacher, D. ; Philippaert, K. ; Camacho-Londoño, J.E. ; Mathar, I. ; Dieterich, C. ; Klugbauer, N. ; Biel, M. ; Wahl-Schott, C. ; Lipp, P. ; Flockerzi, V. ; Zischka, H. ; Algül, H. ; Lechner, S.G. ; Lesina, M. ; Grimm, C. ; Fakler, B. ; Schulte, U. ; Muallem, S. ; Freichel, M.

OCaR1 endows exocytic vesicles with autoregulatory competence by preventing uncontrolled Ca2+ release, exocytosis, and pancreatic tissue damage.

2023 Scientific Article in Gastroenterology

Einer, C. ; Munk, D.E. ; Park, E. ; Akdogan, B. ; Nagel, J. ; Lichtmannegger, J. ; Eberhagen, C. ; Rieder, T. ; Vendelbo, M.H. ; Michalke, B. ; Wimmer, R. ; Blutke, A. ; Feuchtinger, A. ; Dershwitz, P. ; DiSpirito, A.M. ; Islam, T. ; Castro, R.E. ; Min, B.K. ; Kim, T.W. ; Choi, S. ; Kim, D. ; Jung, C. ; Lee, H. ; Park, D. ; Im, W. ; Eun, S.Y. ; Cho, Y.H. ; Semrau, J.D. ; Rodrigues, C.M.P. ; Hohenester, S. ; Damgaard Sandahl, T. ; DiSpirito, A.A. ; Zischka, H.

ARBM101 (Methanobactin SB2) drains excess liver copper via biliary excretion in Wilson's disease rats.

2023 Scientific Article in Nature Communications

Schwarz, M. ; Meyer, C.E. ; Löser, A. ; Lossow, K. ; Hackler, J. ; Ott, C. ; Jager, S. ; Mohr, I. ; Eklund, E.A. ; Patel, A.A.H. ; Gul, N. ; Alvarez, S. ; Altinonder, I. ; Wiel, C. ; Maares, M. ; Haase, H. ; Härtlova, A. ; Grune, T. ; Schulze, M.B. ; Schwerdtle, T. ; Merle, U. ; Zischka, H. ; Sayin, V.I. ; Schomburg, L. ; Kipp, A.P.

Excessive copper impairs intrahepatocyte trafficking and secretion of selenoprotein P.

Contact

Prof. Dr. rer. nat. Hans Zischka

Group Leader Oxidative Cell Death