Federico Pietrocola

Federico Pietrocola is a Principal Researcher at the Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm. He leads the Cellular Stress in Health and Disease research group, focusing on molecular mechanisms linking cellular senescence, autophagy, and aging pathologies. His work bridges basic science with translational applications in cancer, metabolic disorders, and fibrotic diseases.

His research investigates cellular senescence as a driver of age-related pathologies and autophagy as a protective mechanism. Key areas include:

• Senescence-induced fibrosis in lung and kidney diseases
• Immunogenic properties of senescent cells in cancer immunity
• Polyamine metabolism (e.g., spermidine) in longevity
• Metabolomic regulation of stress responses
• Senolytic drug development targeting ACBP/DBI and COPI pathways

Analysis of recent publications (2023-2025) reveals a dominant focus on senescence-immune interactions and metabolism-targeted therapies. His group pioneered senolytic screening methods and demonstrated how senescent cells trigger lung fibrosis in humanized models. Strong emphasis on translating findings into treatments for fatty liver disease, chronic kidney disease, and cancer via autophagy modulation.

Scientific Awards:

• No awards listed in provided profile information

Dr. Pietrocola currently directs a major Swedish Research Council grant (2024-2027) for senescence-targeted cancer immunotherapy. He secured consecutive Novo Nordisk Foundation grants (2021-2023) targeting polyamine metabolism in senescence-related disorders. His earlier project (2020-2023) explored immune checkpoint therapies against aging pathologies. While specific students aren't named, his publications indicate active mentorship through collaborative projects.

His Cellular Stress in Health and Disease group develops innovative models including humanized pulmonary fibrosis systems and metabolomic platforms for single-cell analysis. Current work emphasizes senescence-specific immune checkpoints, microvascular aging in kidney disease, and polyamine-based interventions to counteract tissue degeneration across multiple disease contexts.