Our scientific interests are closely tied to autophagy, the main recycling system of the cell. Autophagy regulates fundamental metabolic functions and is disrupted in diseases like ageing, obesity, and neurodegenerative disorders. Our final goal is the understanding of the link between altered autophagy and disease to pave the way for effective treatments. Particularly, we aim to study the relationship between autophagy and lipid metabolism. We have learnt how physiological adaptations, like lipophagy (selective degradation of lipids by autophagy) can provide energy and favor survival, preventing disease (DOI: https://doi.org/10.1002/hep.32048).

In our current main project, we are focusing on macrophage differentiation (M1 and M2) and how lipophagy modulates these changes. M1 macrophages are pro-inflammatory and, in many diseases, considered hurtful but M2 are anti-inflammatory and present beneficial properties. The metabolic phenotype and cytokine profile in both types of activation are quite well known. However, the molecular process that triggers the switch remains obscure. We are providing novel insights to unravel the required molecular and cellular changes to switch from M1 to M2 macrophages. Our project will point to novel targets to modulate immune activation, providing the basis for treatments for alcoholic steatohepatitis and other diseases such as non-alcoholic fatty liver, fibrosis, cirrhosis, and obesity.

Working model. Boosting lipophagy will switch macrophages from M1 to M2 phenotype fostering an anti-inflammatory environment and ameliorating the etiopathology of alcoholic steatohepatitis (ASH).

Our group counts with great experience in the autophagy and lipophagy fields ( https://doi.org/10.1080/15548627.2020.1797280; https://doi.org/10.1080/15548627.2015.1100356) and knowledge of different research models, including in vitro, ex vivo, in vivo (e.g. mice, hamster, zebrafish, flies…)