Mitochondrial Dysfunction, Cancer Research, Aging
Mitochondrial dysfunction affects a wide range of human pathologies, including cancer, aging, metabolic and cardiovascular disease. Understanding how this puzzle works is the challenge of our research. The research interests of my laboratory focus on the role of mitochondria in pathological conditions. Mitochondria are amazing organelles that we inherited from prokaryotic cells about a couple of billion years ago. Since then, they have been living in the big eukaryotic house, helping us to breathe, and paying for housing with the universal biological currency, ATP. They are also the main source of generation of reactive oxygen species (ROS), which play a regulatory role in the process of life and natural cell death. As we age, mitochondrial function progressively deteriorates. Mitochondria lose their respiratory activity, damage accumulates in their mitochondrial genome, and excessive amounts of ROS are produced. Between 30 and 70 years of age, on average, mitochondrial function decreases by 30% in humans, and mutations in mitochondrial DNA and dysregulation of mitochondrial metabolism are often harbingers of cancer, cardiovascular and neurodegenerative diseases. Over time, our organs age differently and therefore, with the same chronological age, the biological age of our mitochondria in them is also different, which manifests itself in a different set of mitochondrial dysfunctions. We are conducting research in several areas:
1. Studying the effects of repurposed drugs that cause mitochondrial dysfunction on a specific subpopulation of cancer-resistant and cancer stem cells, as part of anticancer therapy;
2. Study of the molecular mechanisms of mitochondrial function in pathologies associated with aging, in particular, Parkinson’s disease;
3. Development of screening systems to detect side effects of drugs and contaminants associated with mitochondrial damage;
4. Studying the horizontal mitochondrial transfer from cell to cell through extracellular vesicles and tunneling nanotubes.
Models: primary and immortal cells, mice, Armemia salina
Collaborations: Department of Epidemiology and Biostatistics, Schulich School of Medicine and Dentistry, Western University, London, Canada
Department of Biological Sciences, University of Illinois at Chicago, Chicago, USA
Department of Chemical Sciences, Federico II Naples University, Naples, Italy.