Jorge Montesinos

This study shows that cholesterol availability through HDLs and SR-B1 drives MAM formation, which regulates ER-mitochondria communication and cholesterol metabolism.

This study identifies cholesterol accessibility as a key driver of TLR4-dependent microglial activation, showing that SR-B1 mediates LPS-induced cholesterol uptake and regulates TLR4 signaling and inflammatory responses.

This study identifies how a single mutation in the Omicron variant of SARS-CoV-2's ORF3a protein alters its host-cell remodelling effects, shifting from lipid accumulation to preserving Golgi structure.

This study identifies the resolvin D and E biosynthesis pathway as activated in cellular senescence and ageing, with its knockdown impairing senescence induction.

This study identifies how C99 disrupts ACSL4 activity and phospholipid homeostasis in Alzheimer's disease by remodeling MAMs and altering PC composition.

This study shows that SR-B1-mediated cholesterol uptake from HDL stimulates MAM formation, which suppresses de novo cholesterol biosynthesis.

This study shows that disrupted MAM function in ALS models leads to altered mitochondrial metabolism, specifically a shift from pyruvate to fatty acid utilization.

This study shows that the C99 fragment of APP regulates cholesterol trafficking between the plasma membrane and ER, contributing to AD pathogenesis.