Research Group Mitochondrial Toxicology
Zischka GroupWe 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 Publications
Read more2024 Scientific Article in Muscle & Nerve
Amyotrophic Lateral Sclerosis and swim training affect copper metabolism in skeletal muscle in a mouse model of disease.
2024 Review in International Journal of Molecular Sciences
Metabolic derangement of essential transition metals and potential antioxidant therapies.
2024 Scientific Article in Analytical and Bioanalytical Chemistry
Subzero project: Comparing trace element profiles of enriched mitochondria fractions from frozen and fresh liver tissue.
2024 Scientific Article in Metabolism: clinical and experimental
Copper impairs the intestinal barrier integrity in Wilson disease.
2024 Scientific Article in ChemBioChem
Thermal proteome profiling reveals insight to antiproliferative and pro-apoptotic effects of Lagunamide A in the modulation of DNA damage repair.
2024 Scientific Article in Journal of Clinical Investigation
OCaR1 endows exocytic vesicles with autoregulatory competence by preventing uncontrolled Ca2+ release, exocytosis, and pancreatic tissue damage.
2024 Scientific Reports
Correction to: A fluorometric assay to determine labile copper(II) ions in serum (Scientific Reports, (2023), 13, 1, (12807), 10.1038/s41598-023-39841-9).
2024 Scientific Article in Biochimica et Biophysica Acta - Molecular Basis of Disease
Amyotrophic lateral sclerosis associated disturbance of iron metabolism is blunted by swim training-role of AKT signaling pathway.
2023 Scientific Article in Gastroenterology
ARBM101 (Methanobactin SB2) drains excess liver copper via biliary excretion in Wilson's disease rats.
2023 Scientific Article in Nature Communications
Farnesoid X receptor activation by bile acids suppresses lipid peroxidation and ferroptosis.
2023 Scientific Article in Nature Communications
Excessive copper impairs intrahepatocyte trafficking and secretion of selenoprotein P.
2023 Scientific Article in Acta Crystallographica Section F