Silvia Maglioni

This study shows that loss of mitochondrial glutathione reductase and thioredoxin reductase in C. elegans causes growth, fertility, and muscle defects, activates a constitutive UPRmt, and alters mitochondrial morphology.

This study identifies fard-1 and dhs-25 as regulators of ferroptosis-driven aging in C. elegans by linking redox imbalance to oxidative stress and lifespan reduction.

This study develops a C. elegans model expressing a human amyloidogenic light chain to study cardiac tropism in AL amyloidosis, finding pharyngeal impairment and oxidative stress similar to human cardiac disease.

The paper identifies that lysosomal defects up-regulate cholesterol synthesis via mitochondrial respiratory chain interactions and Ca2+ retention, while mitochondrial defects down-regulate it.

This study identifies lutein as a potential therapeutic for mitochondrial dysfunction-induced neurodevelopmental defects in C. elegans by restoring neuroligin expression.