Diploma Study of Pharmacy,
Topic: Role of aldehyde dehydrogenase-2 localization in nitroglycerin-induced vasodilation,
passed with distinction
Mitochondrial (Dys)FunCtion
in Aging and diseases
We explore how mitochondria function – and sometimes fail – during aging, in age-related diseases, and in Dravet syndrome.
Using cutting-edge fluorescence microscopy, we study signal pathways in a range of experimental systems, from cellular aging models and cancer cells to patient-derived cells and nematodes (Caenorhabditis elegans).
Our ultimate goal is to turn these insights into new strategies to keep cells healthier for longer and to improve treatments for age-related diseases, cancer, and Dravet syndrome.
Corina Madreiter-Sokolowski
Associate Professor
As an Associate Professor at the
Molecular Biology and Biochemistry at the Medical University of Graz, Corina Madreiter-Sokolowski focuses on understanding mitochondrial function in aging and diseases.
With a background in pharmacy and extensive international experience at renowned institutions like ETH Zurich, Corina Madreiter-Sokolowski leads a research group dedicated to developing innovative strategies to improve health across the lifespan.
2008 – 2012
2012 – 2016
FWF-funded Ph.D. Student
in the laboratory of Prof. Dr. Wolfgang F. Graier,
Institute of Molecular Biology and Biochemistry,
Medical University of Graz (Austria),
passed with distinction
2013
Guest Scientist
at Les Laboratoires Servier, Paris (France),
Topic: Aging model of porcine aortic endothelial
2016 – 2018
University Assistant
in the laboratory of Prof. Dr. Wolfgang F. Graier,
Gottfried Schatz Research Center,
Medical University of Graz (Austria)
2018
Regulatory Affairs Assistant,
Gerot Lannach Pharma, Lannach (Austria)
2018 – 2020
FWF-funded Project Leader
in the laboratory of Prof. Dr. Michael Ristow,
ETH Zurich (Switzerland),
Topic: Mitochondrial calcium homeostasis and aging
2020
Guest Scientist
in the laboratory of Prof. Dr. Pidder Jansen-Dürr,
University of Innsbruck (Austria),
Topic: Establishment of an in vitro aging model based on fibroblasts
2020 – 2022
Assistant Professor (§99/5) for „Molecular Aging“,
Gottfried Schatz Research Center,
Medical University of Graz (Austria)
2021
Venia docendi for Molecular Biology and Biochemistry,
Medical University of Graz (Austria),
Title: The function of mitochondria and their role in aging-associated diseases
2022
EMBO-funded Guest Scientist
in the laboratory of Prof. Dr. Sabrina Büttner,
Stockholm University (Austria),
Topic: Studying mitochondrial calcium in yeast
2022 – today
Associate Professor (§99/5) for „Molecular Aging“,
Gottfried Schatz Research Center,
Medical University of Graz (Austria)
Award-winning science
Corina Madreiter-Sokolowski’s research in mitochondrial function in aging and diseases has been honored with numerous prestigious awards. Highlights include the 2017 Award of Excellence from the Federal Ministry of Education, Science and Research, the 2022 Elisabeth Lutz Prize from the Austrian Academy of Sciences (ÖAW), and the 2021 GRAWE Award from Graz Mutual Insurance Company.
She has also received the 2018 Erwin Schrödinger Abroad Fellowship from the Austrian Science Fund (FWF), the 2022 Scientific Exchange Grant from EMBO, and the 2023 Josef Krainer Award. These accolades reflect her dedication to advancing scientific knowledge and excellence.
Award of Excellence
Federal Ministry of Education, Science and Research
Elisabetz Lutz Prize
Austrian Academy of Sciences (ÖAW)
Grawe Award
Graz Mutual Insurance Company
all Awards
2023 Josef Krainer Würdigungspreis
2022 Scientific Exchange Grant – European Molecular Biology Organization (EMBO)
2022 Preidler/Szolar Fellowship – MEFOgraz
2022 Elisabeth Lutz Prize – Austrian Academy of Sciences (ÖAW)
2021 GRAWE Award 2021 – Graz Mutual Insurance Company (GRAWE)
2018 Erwin Schrödinger Abroad Fellowship (stay-abroad at the ETH Zurich) – Austrian Science Fund (FWF)
2017 Sanofi Research Prize – Sanofi
2017 Comprehensive Cancer Center (CCC) Thesis Award
2014 Poster Prize Cardiovascular Research Doc Day
Our Research
Promotion of lifespan by mitochondrial Calcium and ROS homeostasis
Reactive oxygen species (ROS) play a dual role in cellular biology: they are essential for signal transduction but can cause significant damage when present in excess. In this project, we use nematodes (Caenorhabditis elegans) and cellular aging models to explore how mitochondrial calcium regulation influences ROS levels. Our goal is to uncover mechanisms that modulate ROS in a targeted way, promoting lifespan extension and improved fitness in old age. For more information about our project, please visit the FWF Research Radar.
Interorganellar communication in cellular senescence
The FWF research group SENIOPROM is dedicated to uncovering the mechanisms driving cellular senescence. Our focus includes mitochondrial function, interactions between mitochondria and other organelles, metabolic regulation, and the maintenance of functional proteins. By understanding these processes, we aim to lay the foundation for new therapeutic strategies to selectively eliminate senescent cells, ultimately contributing to healthier aging and improved quality of life. For more information about our project, please visit the FWF Research Radar.
T3-induced rewiring of mitochondrial calcium in cancer cells
Thyroid hormones are master regulators of cellular metabolism and play a critical role in cancer cells, which depend on energy to support their invasive growth. We study how thyroid hormones influence mitochondrial calcium homeostasis, thereby impacting mitochondrial function and energy production in various cancer cell types. For more information about our project, please visit the FWF Research Radar.
Mitochondrial (dys)function in Dravet syndrome
Dravet syndrome is a severe, early-onset epileptic encephalopathy. We focus on understanding how impaired mitochondrial function affects energy metabolism, cellular signaling, and overall cellular health. By unraveling these mechanisms, we aim to identify potential therapeutic targets that could mitigate mitochondrial dysfunction and improve outcomes for individuals with Dravet syndrome. For more information about our project, please visit the FWF Research Radar.
Our Publications
Explore our recent research dedicated to mitochondrial function in aging and diseases. Our work, published in leading scientific journals, showcases discoveries and innovative approaches. Stay updated with our latest findings and contributions to the scientific community through our comprehensive publication list on PubMed.
Bresilla D, Tawfik I, Hirtl M, Gabrijelčič S, Ostaku J, Mossegger F, Wurzer L, Lederer S, Kalinova K, Malle E, Schosserer M, Zarse K, Ristow M, Madreiter-Sokolowski CT. Enhancing late-life survival and mobility via mitohormesis by reducing mitochondrial calcium levels. Aging Cell. 2025. DOI: 10.1111/acel.70247
Reducing mitochondrial calcium uptake in C. elegans – either by knocking down the uniporter gene mcu-1 or by the drug mitoxantrone – triggers a transient ROS signal that activates stress-response pathways (pmk-1/p38, daf-16/FOXO, skn-1/NRF2), preserves mitochondrial structure and function, and thereby extends lifespan and late-life mobility.
Kalinová K, Gottschalk B, Hirtl M, Ostaku J, Gabrijelčič S, Sokolowski A, Malle E, Graier WF, Madreiter-Sokolowski CT. Targeting enhanced mitochondrial respiration chain activity as a potential therapeutic approach for endometriosis. Biochim Biophys Acta Mol Basis Dis. 2025. DOI: 10.1016/j.bbadis.2025.167885
We showed that endometriotic 12Z cells share cancer cell-like mitochondrial structural changes and vulnerabilities, with a unique reliance on reverse FOF1-ATP synthase activity and electron transport chain function, suggesting these as potential therapeutic targets for endometriosis.
Tawfik I, Schlick K, Ostaku J, Bresilla D, Gabrijelčič S, Gottschalk B, Sokolowski A, Malle E, Kalinova K, Hirtl M, Madreiter-Sokolowski CT. Breast cancer cells utilize T3 to trigger proliferation through cellular calcium modulation. Cell Communication and Signaling. 2024. DOI: 10.1186/s12964-024-01917-y
We discovered that breast cancer cells harness T3 to upregulate IP3R3 through THRα, enhancing mitochondrial Ca²⁺ uptake and driving cancer cell metabolism and proliferation.
Bresilla D, Habisch H, Pritišanac I, Zarse K, Parichatikanond W, Ristow M, Madl T, Madreiter-Sokolowski CT. The sex-specific metabolic signature of C57BL/6NRj mice during aging. Scientific Reports. 2022. DOI: 10.1038/s41598-022-25396-8
We revealed that age-related metabolic alterations emerge as early as 6 months in mice, often exhibiting a biphasic pattern.
Tawfik I, Gottschalk B, Jarc A, Bresilla D, Rost R, Obermayer-Pietsch B, Graier WF, Madreiter-Sokolowski CT. T3-induced enhancement of mitochondrial calcium uptake as a boost for mitochondrial metabolism. Free Radical Biology and Medicine. 2022. DOI: 10.1016/j.freeradbiomed.2022.01.024
We discovered that cancer cells leverage T3 to rewire mitochondrial calcium homeostasis by specifically upregulating UCP2.
Tian J, Geiss C, Zarse K, Madreiter-Sokolowski C*, Ristow M. Green tea catechins EGCG and ECG enhance the fitness and lifespan of Caenorhabditis elegans by complex I inhibition. Aging (Albany NY) . 2021. DOI: 10.18632/aging.203597
We demonstrated that green tea catechins induce a mitohormetic response by inhibiting complex I of the electron transport chain, thereby promoting health and extending lifespan in C. elegans.
Madreiter-Sokolowski CT, Gottschalk B, Sokolowski AA, Malli R, Graier WF. Dynamic control of mitochondrial calcium levels as a survival strategy of cancer cells. Frontiers in Cell and Developmental Biology. 2021. DOI: 10.3389/fcell.2021.614668
We found that cancer cells dynamically modulate the interaction between mitochondria and the endoplasmic reticulum, which inversely correlates with the expression of mitochondrial calcium uptake proteins.
Gottschalk B, Klec C, Leitinger G, Bernhart E, Rost R, Bischof H, Madreiter-Sokolowski CT, Radulovic S, Eroglu E, Sattler W, Waldeck-Weiermair M, Malli R, Graier WF. MICU1 controls cristae junction and spatially anchors mitochondrial calcium uniporter complex. Nature Communications. 2019. DOI: 10.1038/s41467-019-11692-x
We revealed that MICU1, the mitochondrial calcium gatekeeper, anchors MCU and EMRE at the inner boundary membrane in response to elevated calcium levels.
Madreiter-Sokolowski CT*, Waldeck-Weiermair M, Bourguignon MP, Villeneuve N, Gottschalk B, Klec C, Stryeck S, Radulovic S, Parichatikanond W, Frank S, Madl T, Malli R, Graier WF. Enhanced inter-compartmental calcium flux modulates mitochondrial metabolism and apoptotic threshold during aging. Redox Biology. 2019. DOI: 10.1016/j.redox.2018.11.003
We discovered that senescent cells exhibit an enhanced physical interaction between mitochondria and the endoplasmic reticulum, rendering them particularly susceptible to mitochondrial calcium-overload provoking agents such as resveratrol.
Madreiter-Sokolowski CT, Györffy B, Klec C, Sokolowski AA, Rost R, Waldeck-Weiermair M, Malli R, Graier WF. UCP2 and PRMT1 are key prognostic markers for lung carcinoma patients. Oncotarget. 2017.DOI: 10.18632/oncotarget.20571
We demonstrated that cancer cells with concurrent upregulation of UCP2 and PRMT1 exhibit enhanced metabolism, a condition associated with reduced survival probability in lung cancer patients with co-expression of these genes.
Madreiter-Sokolowski CT, Klec C, Parichatikanond W, Stryeck S, Gottschalk B, Pulido S, Rost R, Eroglu E, Hofmann N, Bondarenko A, Madl T, Waldeck-Weiermair M, Malli R, Graier WF. PRMT1-mediated methylation of MICU1 determines the UCP2/3-dependency of mitochondrial calcium uptake in immortalized cells. Nature Communications. 2016. DOI: 10.1038/ncomms12897
We discovered that PRMT1-mediated methylation of MICU1 impairs mitochondrial calcium uptake, a dysfunction counteracted by UCP2 in cancer cells.
Madreiter-Sokolowski CT, Gottschalk B, Parichatikanond W, Eroglu E, Klec C, Waldeck-Weiermair M, Malli R, Graier WF. Resveratrol specifically kills cancer cells by a devastating increase in the calcium coupling between the greatly tethered endoplasmic reticulum and mitochondria. Cellular Physiology and Biochemistry. 2016. DOI: 10.1159/000447844
We found that resveratrol-induced ATP synthase inhibition reduces cellular ATP levels, impairing SERCA activity and leading to mitochondrial calcium overload.
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