Selected publications
Corina Madreiter-Sokolowski is an Associate Professor for "Molecular Aging" at the Medical University of Graz (Austria). Her main interest is the function of mitochondria in longevity. As a pharmacist searching for novel anti-aging strategies, she studies mitochondrial metabolism, calcium handling, and reactive oxygen species (ROS) homeostasis in age-related diseases.
Corina Madreiter-Sokolowski
Additionally: ORCID.
(1) Tawfik I, Gottschalk B, Jarc A, Bresilla D, Rost R, Obermayer-Pietsch B, Graier WF, Madreiter-Sokolowski CT*. T3- induced enhancement of mitochondrial Ca2+ uptake as a boost for mitochondrial metabolism. Free Radic Biol Med 2022; doi: 10.1016/j.freeradbiomed.2022.01.024.
We identified mitochondrial calcium modulation as crucial action of T3 to modulate mitochondrial metabolism.
(2) Tian J, Geiss C, Zarse K, Madreiter-Sokolowski CT*, 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 revealed the intracellular signaling cascade how green tea catechins prolong life- and healthspan.
(3) Madreiter-Sokolowski CT, Gottschalk B, Sokolowski AA, Malli R, Graier WF. Dynamic control of mitochondrial Ca2+ levels as a survival strategy of cancer cells. Front Cell Dev Biol 2021; doi: 10.3389/fcell.2021.614668.
We identified the interplay between UCP2 and MAM formation in cancer cells.
(4) Madreiter-Sokolowski CT, Thomas C, Ristow M. Interrelation between ROS and Ca2+ in aging and age-related diseases. Redox Biol 2020;36:101678. doi: 10.1016/j.redox.2020.101678.
In this paper, we elaborated the interrelation between ROS and Ca2+ in aging and its implication in age-related diseases.
(5) 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 Ca2+ uniporter complex. Nat Commun 2019;10(1):3732. doi: 10.1038/s41467-019-11692-x.
We used cutting-edge, high-resolution microscopy to unveil MICU1’s control of cristae junction.
(6) 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 Ca2+ flux modulates mitochondrial metabolism and apoptotic threshold during aging. Redox Biol 2019;20:458-466. doi: 10.1016/j.redox.2018.11.003.
We used the PAEC in vitro aging model to reveal age-related changes in the interorganelle communication between ER and mitochondria.
(7) Alkan HF, Walter KE, Luengo A, Madreiter-Sokolowski CT, Stryeck S, Lau AN, Al-Zoughbi W, Lewis CA, Thomas CJ, Hoefler G, Graier WF, Madl T, Vander Heiden MG, Bogner-Strauss JG. Cytosolic aspartate availability determines cell survival when glutamine is limiting. Cell Metab 2018;28(5):706-720.e6. doi: 10.1016/j.cmet.2018.07.021.
We presented the control of cytosolic aspartate on cell survival.
(8) 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;8(46):80278-80285. doi: 10.18632/oncotarget.20571.
We used a bioinformatical approach and the TCGA database to investigate the impact of two proteins controlling Ca2+ homeostasis on the prognosis of lung carcinoma patients.
(9) 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 Ca2+ uptake in immortalized cells. Nat Commun 2016;7:12897. doi: 10.1038/ncomms12897.
In this paper, we revealed a new control mechanism of mitochondrial Ca2+ uptake.
(10) Madreiter-Sokolowski CT, Gottschalk B, Parichatikanond W, Erogul E, Klec C, Waldeck-Weiermair M, Malli R, Graier WF. Resveratrol specifically kills cancer cells by a devastating increase in the Ca2+ coupling between the greatly tethered endoplasmic reticulum and mitochondria. Cell Physiol Biochem 2016;39(4):1404-20. doi: 10.1159/000447844.
We showed a mechanism for Resveratrol’s action as an anti-cancer drug.