Portraits of Young Researchers: Sonny YDE

Understanding Mitochondrial Dysfunction in MASLD

Sonny YDE

UMRS1166 – Team 5 – Metabolic Diseases, Diabetes, and Comorbidities – Fabienne Foufelle, Frédéric Jaisser – Pitié-Salpêtrière, Paris
UMR3691 – Research Team – Mitochondrial Biology, Timothy WAI, Institut Pasteur, Paris

Awards Received / Honors

• 2022: Ministerial Ph.D. Fellowship, Doctoral School 394
• 2024: Best Scientific Poster Award, ICAN and CMDO Winter Camp, Canada
• 2024: Award for Best Scientific Statement of Purpose, ICAN and CMDO Winter Camp, Canada
• 2025: Best Scientific Poster Award, IHU ICAN Scientific Day
• 2025: Welding Scholarship Awarded by the Pasteur Institute

Major Publications

• Patitucci, C., Hernández-Camacho, J.D., Vimont, E., et al. Mtfp1 ablation enhances mitochondrial respiration and protects against hepatic steatosis. Nat Commun 14, 8474 (2023).
• Yde, S., Patitucci, C., et al. Mtfp1 influences MASH severity in a sex-dependent manner in mice. In preparation.

Training

• Curious to understand how biological mechanisms influence health and contribute to the development of diseases, I have built my career around biomedical research. After earning a BTS in Biotechnology followed by a Bachelor’s degree in Biomedical Research, my internships allowed me to explore several experimental models, ranging from thyroid development to the biology of pancreatic β-cells, to neurodegenerative mechanisms in C. elegans.
• These experiences have strengthened my desire to understand how cellular and molecular dysregulations can lead to human diseases.
• My master's degree in life sciences, followed by a focus on molecular and cellular biology, led me to study mitochondria in neurodegenerative and then liver diseases.
• Today, my doctoral research on mitochondrial dysfunction in NAFLD builds on this work, with the goal of better understanding the mechanisms involved in these chronic diseases.

Research Project

• Metabolic and fatty liver disease (MASLD) is the most common chronic liver disease worldwide. It is characterized by increased fat accumulation that can progress to non-alcoholic steatohepatitis (NASH) with inflammation, hepatocyte damage, and fibrosis, which can lead to cirrhosis or liver cancer.
• I am studying the role of mitochondria—and specifically the mitochondrial protein MTFP1—in this process. Deletion of Mtfp1 in hepatocytes protects males against steatosis and liver damage on a high-fat diet. I therefore studied MASH-inducing diets to determine whether this protection extends to more advanced stages of NASH.
• My research shows that the absence of MTFP1 protects only males against liver damage and cell death, without significantly reducing steatosis and MASH. These results suggest that MTFP1 regulates distinct mitochondrial functions that are modulated by sex.