NADIS 1.0 Interview: Eija Pirinen
Could you tell us about your scientific journey and what inspired you to investigate the connection between mitochondria signalling and disease?
Eija: Well, my mitochondria-related scientific journey started during my PhD studies, when I was investigating mice with accelerated polyamine catabolism. I came across a striking finding that these mice were resistant to diet-induced obesity.
I then noticed that the mechanism behind this was most likely the beiging of white adipose tissue — a process in which mitochondrial number and activity increase. This was a really fascinating and unexpected discovery, and it sparked my interest in mitochondria.
Since then, I have been focusing on understanding the signalling and mechanisms underlying mitochondrial dysfunction, and how mitochondrial function and health contribute to whole-body energy metabolism. It has been fascinating to follow how profoundly mitochondrial health impacts overall metabolic health in humans.
So, connecting these findings a bit to the models you’re using — especially the development of 3D spheroid models — what do you see as the main advantages of these models? And how do they help you study obesity in ways that weren’t possible before?
Eija: The critical gap in the obesity research and drug development has been the lack of physiological in vitro study models for human adipocytes. And we have now developed a 3D culture model for human adipocyte spheroids and optimized it specifically to study mitochondrial function. We refined the spheroid size so that we can perform analyses such as Seahorse measurements — in other words, assessments of mitochondrial respiration. This was a key step that now allows us to begin addressing one of the major unanswered questions: what causes mitochondrial dysfunction in adipocytes during obesity.
And now, we can also use this model to identify new mitochondrial activators. This is one of its main advantages — it allows us to better understand what happens in adipocytes in the context of obesity.
Exciting! As a principal investigator in the NADIS network, how does the collaborative environment help you to accelerate your research in the training of the next generation of scientists?
Eija: From my perspective, being part of the NADIS consortium has really accelerated my research and my lab’s work. It has been wonderful to share data so easily and quickly. We can exchange tools and methods, and — even more importantly — plan new experiments together and discuss what our results mean and what to do next.
This kind of collaboration is really valuable, especially since in Finland we have often worked in isolation. Now, having all these collaborators to truly work together is fantastic — it’s a huge asset and has helped us a lot.
For student training, the benefits are similar. The students gain new technical skills in different labs, and, just as importantly, they learn to communicate and work within diverse scientific and cultural environments. That’s an essential part of their development as researchers.
And if you were to continue this European collaboration, such as in the form of NADIS 2.0, what would be the key questions you would like to address, particularly regarding mitochondrial health and its link to human disease?
Eija: I think it’s still very important to continue studying the mechanisms that lead to mitochondrial dysfunction and NAD⁺ deficiency, because we still don’t fully understand them.
The reason I want to keep investigating these mechanisms is that we need to design targeted treatments. We shouldn’t apply NAD⁺ boosters randomly to all diseases — we need to understand the underlying biology before developing therapies.
What I really hope is that, within NADIS 2.0, we can start developing disease- and context-specific treatments based on this deeper understanding.
Thank you, Eija.