Tetiana Yatsenko
Fellow 2025/2026
Chemistry
Palladin Institute of Biochemistry of NAS of Ukraine
Volkswagen Stiftung
tetyanaa.yatsenko@gmail.com
Bio
Tetiana Yatsenko is a Senior Researcher at the Palladin Institute of Biochemistry of the National Academy of Sciences of Ukraine, where she also serves as Head of the Young Scientists Council. She graduated with a Master’s degree in Biology from Donetsk National University in 2011 and earned her PhD in Biochemistry from the Palladin Institute in 2018. From 2016 to 2020, she co-founded and acted as Scientific Advisor for the biotech start-up BIOsens. Her international research experience includes visiting scholar positions at Juntendo University (Japan), the Kielanowski Institute of Animal Physiology and Nutrition (Poland), and Lund University (Sweden).
Her research focuses on enzyme chemistry, molecular biology, fibrinolysis-related pathologies, and the molecular mechanisms of plasminogen activation. She applies a wide range of laboratory methods, including protein isolation and characterization, ELISA, Western blotting, flow cytometry, qPCR, DNA sequencing, and animal model studies. She is certified in laboratory animal handling by ARPIN (Japan) and PolLASA (Poland).
Tetiana is the author of 18 research papers and 4 patents (as of November 2024). She has received numerous awards and grants, including the Horizon 2020 SME Instrument Grant for BIOsens, the NASU Grant for young scientists, the Scholarship of the President of Ukraine for Young Scientists, the Prize of the Verkhovna Rada of Ukraine for young scientists (2023), and the JSPS Postdoctoral Fellowship (2022–2024).
Investigation of the molecular and genetic regulation of PAI-1 expression hyperosmotic stress response
The proposed project aims to unravel the complex mechanisms underlying hyperosmotic stress responses in normal and cancer cells, and their impact on fibrosis regulation. Preliminary data linking genetics, cell signaling, and disease gives a novel perspective on how hyperosmotic stress influences cellular processes. This work has the potential to describe a new regulatory pathway involved in tissue fibrosis, diabetes, or chronic kidney disease and develop approaches for pathway modulation and stress response correction for clinical practice. Ultimately, it may help to create a personalized predictive approach based on patient genotyping.
Hyperosmotic stress poses a risk for the development of inflammatory disorders, hypertension, endothelial dysfunction, fibrosis, and thrombosis. PAI-1, an essential regulator of fibrinolysis and proteolysis, is one of the main fibrogenesis-related factors induced by hyperosmolarity and inflammation. Upregulation of PAI-1 driven by inflammation through NFκB depends on the 4G/5G polymorphism in the PAI-1 promoter gene, with significant clinical implications for delayed fibrinolysis and thrombotic risks.
Building upon our preliminary data, we hypothesize that hyperosmolarity- and inflammation-responsive transcriptional factor NFAT5 due to its structural similarity to NFκB might differentially activate PAI-1 expression depending on the 4G or 5G promotor variant and drugs targeting NFκB/NFAT5 pathways can modulate hyperosmolarity-induced PAI-1 expression based on the 4G/5G polymorphism. This project aims to define the signaling pathways transcription factors (NFAT5, NFκB, KLF2) controlling PAI-1 expression in cells under hyperosmotic stress, considering genetic variations in the PAI-1 promoter region (4G/5G polymorphism). Additionally, we will explore the prognostic implications of 4G/5G genotyping for personalized therapy targeting PAI-1-related complications like thrombosis or fibrosis.