Why did you move to Sweden after your PhD in Belgrade?
I was born in the small coastal town of Bar in Montenegro when it was still part of Yugoslavia. I feel strongly connected to the whole region as my mother and father have roots in Montenegro, Northern Macedonia and Croatia, and I studied and spent a lot of time in Serbia. I moved to Belgrade for my university studies in the 1990s, a time when Yugoslavia was breaking apart and the country was under international sanctions, making it difficult to leave. So, I stayed and completed my PhD there. By the time I finished in 1999 I had just gotten married and together with my husband we decided to move to Sweden – one of the few countries in Europe then offering work permits to both of us.
Sweden didn’t offer opportunities in my original research field, so I had to change my research field entirely. I joined Nils-Göran Larsson’s lab at the Karolinska Institute and began working on mitochondrial biology, a field I knew little about at the time. It was the early 2000s, and transgenic mouse models were a big thing in biomedical research. I helped develop a mouse model for premature aging caused by mitochondrial dysfunction. I was initially drawn in by the cutting-edge technology but soon became completely captivated by the fascinating world of mitochondrial biology. Since then, I have been fully immersed in mitochondrial research, and I truly love it.
To a certain extent moving to Sweden and starting research on mitochondria involved some degree of chance. That is why I always tell people that you do not need to have a completely planned and straightforward career path to succeed in science. It can also sometimes involve a bit of chance and luck.
What prompted you to move to Cologne?
in 2008 I was approached by my colleagues from the University of Cologne and asked if I would be interested in joining a newly established Cologne Excellence Cluster for Aging and Aging-Associated Diseases (CECAD). As my postdoctoral work mainly focused on the role of mitochondria in ageing and ageing-associated diseases, this was a perfect research environment for me to continue my research career. This was in 2009 and we did not regret this decision at all. Our daughter was just three when we moved and she integrated in Germany and Cologne super well.
What is your personal research focus?
I work on understanding mitochondrial function and how it communicates with the rest of the cell. My lab is interested in understanding the signaling pathways in response to mitochondrial dysfunction in the context of aging and different metabolic diseases.
Mitochondria are organelles inside almost every living eukaryotic cell. They are considered the powerhouse of the cell because they produce most of the cell’s energy in the form of ATP. Over the last ten years or so, we started understanding that while the powerhouse aspect is important, there are many other different pathways regulated by mitochondria, which also act as an important signaling hub in the cell.
Mitochondrial dysfunction comes in many flavors and the cell reacts to these perturbations of mitochondrial function in different ways. Those stress responses might be both beneficial and maladaptive, and this is what I am studying in the context of different physiological settings. For example, during development of the skeletal muscle or ischemia reperfusion injuries in the heart or kidney.
Where might your research lead?
We work a lot on mitochondria proteostasis mechanisms by studying various mitochondrial proteases. A big part of our work focuses on understanding how mitochondrial proteases monitor and regulate quality control of respiratory chain (OXPHOS) complexes. We have discovered that, while in normal conditions the removal of faulty OXPHOS complexes keeps energy production intact, in the disease states when the majority of OXPHOS becomes unstable, this surveillance mechanism actually worsens the disease’s phenotypes.
We are now working to develop a screen for a potential inhibitor of this quality control protease. The idea is that in future you can use these inhibitors to treat people who have mitochondrial diseases. We have also discovered this might be important during ischemia and reperfusion that happens during heart attack or stroke. Similarly, ischemia and reperfusion also happens during an organ transplant when you cut the blood supply and keep the organ for some time without oxygen. It is when you replace the oxygen supply that the organ has a sudden oxidative stress and we think we can manipulate these proteins and prevent this.
We think this might be used in future for example in kidney transplants when you could store the kidney in the inhibitor. Most people do not think about transplantation as a problem, but it involves completely cutting oxygen supply to an organ and then having to revive it, which inevitably comes with ischemia-reperfusion injury. We always have this kind of benefit in the back of our mind but my primary driving force is to understand how and why the processes work in this way.
How did you react to election as an EMBO Member?
Becoming a Member is amazing. It is recognition of your work and I was really very proud and happy to hear the news. I attended the Members’ Meeting in 2024 and it was great to meet other Members and talk to different people from different areas of research.
I have also organized several editions of the EMBO-FEBS Lecture Course series on Mitochondrial Biology (Mitochondria in Life, Death, and Disease), which play an important role in our scientific community, particularly for early-career researchers. We make a point of asking invited speakers to provide broad introductions to their fields, ensuring the course is truly educational and inclusive.
The course covers a wide range of topics, from unicellular organisms to plants and humans, and brings together researchers from different disciplines who don’t typically interact. My involvement began in 2002, when my postdoctoral supervisor, originally set to lead a part of EU-funded lecture series on mitochondria, asked me to step in. That experience introduced me to many key members of the field and solidified my commitment to fostering this community.
I’m especially pleased that EMBO continues to support the series, and we are now encouraging younger colleagues to take on organizational roles to ensure the course continues to evolve and thrive.
