Biology of robustness

      We strive to understand the mysteries of two opposing biological phenomena: aging, which is a progressive structural and functional decline of living beings on all levels of organization, and robustness, a natural capacity to resist damage and counteract aging and diseases. 
      Similar age of onset for diverse age-related diseases (ARD) in most humans and the existence of rare “outliers” – centenarians that remain disease-free throughout their lifetime - suggest a common cause, and even mechanism, for all ARD. On the molecular level, oxidative damage to proteins and in particular protein carbonylation lies at the core of aging and ARD. Importantly, protein variants differ in their intrinsic susceptibility to carbonylation, and we are particularly interested in the two extreme ends of the spectra: carbonylation-resistant proteins, and proteins with higher-than-average vulnerability to oxidative damage, such as various disease-associated mutants. The key question is then how such damaged proteins hamper cellular function and kill the cells in degenerative diseases. Furthermore, we are developing novel, nanotechnology-based approaches to detect carbonyls on recombinant proteins and in the cellular environment.
      In the second line of our research, we use bioinformatics and experimental approaches to tackle natural strategies for attenuating age-related deterioration on the level of cell populations and tissues. Age-dependent accumulation of damage in individual cells is a stochastic process and as such leads to a progressive increase in heterogeneity of cells within tissues. Nevertheless, in spite of the increasing number of damaged cells, the tissues remain healthy and functional for decades. This tissue robustness can be explained by cellular parabiosis – healing of highly damaged cells by means of molecular exchange with their healthy neighbors. In addition to its role in sustaining viability of damaged cells, cellular parabiosis could potentially suppress development of cancers, keeping the pioneer malignant cells silent for extended periods of time. 
      The main goal of all our projects is to set basis for development of strategies to attenuate aging and to delay the onset of age-related diseases. 
      The group has been established in 2007 by Prof. Miroslav Radman and is now led by Katarina Trajkovic (as of 2019).


        1. “Cellular parabiosis: the role of cell-to-cell communication in phenotypic suppression” Croatian Science Foundation (CSF/HrZZ) research project (IP-2019-04-3504; funding period: 2020-2023);
        2. Young Researchers’ Career Development Project; Croatian Science Foundation (CSF/HrZZ) (DOK-2020-01-1998; funding period: 2020-2023);
        3. “Deciphering the mechanism of cellular aging: interaction of oxidatively damaged proteins with the cellular membranes”; Marie Skłodowska-Curie Actions/Individual Fellowship (898685 — CarboPore — H2020-MSCA-IF-2019; funding period: 2020-2022);
        4. “A common mechanism of bacterial and human cell death: identification and characterization of cytotoxic protein oligomers leading to permeabilization of the cellular membranes”; CELLS - ALBA Synchrotron and CALIPSOplus (201902353; experiment performed in November 2019).

        Collaborations within funded projects/actions​
        1. “Application of new nanostructured materials in medical diagnostics”; STIM REI (Center of Excellence for Science and Technology, Integration of Mediterranean Region, Research, Innovation, Education) (KK. 0003.; funding period: 2017-2022);
        2. COST Action “ADHEsion GPCR Network: Research and Implementation Set the path for future Exploration” (CA18240; funding period: 2019-2023).
        3. COST action "A sound proteome for a sound body: targeting proteolysis for proteome remodeling" (CA20113; funding period 2021-2025)font>

          Rodolphe Antoine (C.N.R.S. Institut Lumière Matière, Lyon, France)

          Vlasta Bonačić-Koutecký (Center of Excellence for Science and Technology - Integration of Mediterranean Region (STIM) at the University of Split)

          Tanja Dučić (ALBA Synchrotron, Cerdanyola del Valles, Spain)

          Silva Katušić Hećimović (Institute Ruđer Bošković, Zagreb, Croatia)

          Anita Kriško (University Medical Center Goettingen, Germany)

          Milena Ninković (University Medical Center Goettingen, Germany)

          Tatjana Paunesku (Northwestern University, Chicago, USA)

          Eva Žerovnik (Jožef Stefan Institute, Ljubljana, Slovenia)



            We welcome enthusiastic researchers interested in aging and robustness of life to join our team. 


            MedILS, Mestrovicevo setaliste 45
            21000 Split, Croatia