Happy Thursdays with Marta & Valentina

More than a cell cycle regulator: p107 in metabolic liver disease

p107, a member of the pocket protein family, is emerging as a key regulator of hepatic metabolism. Using murine and human models, we show that its inhibition reduces lipid accumulation, ER stress and fibrosis. Our findings indicate a potential role for p107 in the progression of MAFLD.

CV highlights:

I’m a PhD student at the University of Santiago de Compostela (CiMUS), where I study the role of p107 in metabolic liver disease. My research focuses on lipid metabolism, ER stress, and fibrosis, using both murine models and human cell lines. I hold a degree in Biology and a Master’s in Biomedical Research. I’m also a co-author of a peer-reviewed article in the Journal of Endocrinological Investigation (10.1007/s40618-024-02307-4)
 

Marta Varela Miguéns. PhD student, Diabesity Group (P0L3), CiMUS

The lack of ACC2 in hepatic stellate cells induces liver fibrosis through CPT1A 

Acetyl-CoA carboxylase 2 (ACC2) inhibits fatty acid oxidation by producing malonyl-CoA, a CPT1A inhibitor. In this study, we show that ACC2 expression is reduced in activated hepatic stellate cells (HSCs) during liver fibrosis in humans and mice, correlating negatively with the fibrosis stage. Silencing ACC2 activates HSCs in a CPT1A-dependent manner, while ACC2 overexpression prevents their activation. In vivo, we discovered that HSC-specific ACC2 deletion worsens fibrosis. 
These findings suggest that the loss of ACC2 promotes HSC activation via enhanced fatty acid oxidation, contributing to the progression of liver fibrosis.

CV highlights:

• Degree in Biology – University of Santiago de Compostela
• Master's degree in Molecular Neuroscience – University of Santiago de Compostela
• FPI fellowship – Agencia Estatal de Investigación
  
   

Valentina Dorta Bouza. PhD student at the Molecular Metabolism Group (P0L4), CiMUS.

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