NPF-Funded Research

Project Summary:

Psoriasis is a chronic skin disease marked not only by inflammation, but also by altered fat metabolism and oxidative stress. This project asks how a fat-binding protein, called Fabp5, links abnormal lipid handling to ongoing skin inflammation in psoriasis. The aim is to understand how Fabp5 controls fat use and a stress-related cell death process (ferroptosis) in different skin and immune cells. Using mouse models, human data, and pharmacologic treatments, the study will uncover how these processes interact. The findings may reveal new treatment strategies that target metabolic pathways, improving psoriasis care and reducing related metabolic health risks.

How will your project help improve the lives of the 125 million affected by psoriatic disease?

Despite the effectiveness of biologic therapies for psoriasis, a significant subset of patients either fail to respond or relapse over time, representing an important unmet clinical need. This project addresses this gap by investigating how Fabp5-mediated lipid metabolism and peroxidation-specific pathways contribute to psoriasis, extending our understanding of disease mechanisms beyond classical inflammatory pathways. These findings will support the development of metabolic and lipid peroxidation-targeted therapies, and may build a foundation for future work on its cardiometabolic comorbidities.

Why is psoriatic disease research important to you, personally? What role will this award play in your research efforts or career development?

Psoriasis is particularly interesting to me because of its systemic reach - an inflammatory process that originates in the skin but spreads throughout the whole body, affecting distant organs such as the joints, arteries and liver. More specifically, I am interested in the crosstalk between the immune system and metabolism - how inflammatory triggers can drive metabolic responses, and how metabolic changes can, in turn, shape inflammation.

Researcher Profile:

Dr. Kamil Mieczkowski earned his degree from the Intercollegiate Faculty of Biotechnology at the University of Gdansk and Medical University of Gdansk, Poland, where he also completed his PhD investigating the communication between breast cancer cells and their microenvironment. His doctoral work, supported by the National Science Centre's Preludium 12 grant and institutional grants for young scientists, resulted in multiple peer-reviewed publications. He then shifted his research focus to systemic disease mechanisms, joining Erwin Wagner's group at the Medical University of Vienna as a postdoctoral researcher. He was later awarded a prestigious FWF ESPRIT grant to study psoriasis and its systemic comorbidities, including atherosclerosis and metabolic syndrome. Combining genetically engineered mouse models with in vitro, imaging and molecular approaches, his work aims to define how immune-driven skin inflammation rewires metabolic pathways, and more broadly, to understand how chronic inflammatory diseases contribute to systemic comorbidities such as atherosclerosis, metabolic syndrome and psoriatic arthritis.