Ricerc@Sapienza

The Mozzetta Lab investigates the epigenetic mechanisms that regulate skeletal muscle homeostasis, regeneration, and disease. Our research focuses on how chromatin organization, nuclear architecture, and transcriptional networks control muscle stem cells and stromal progenitors, with particular attention to fibro-adipogenic progenitors (FAPs), key regulators of muscle repair and degeneration.

The research group focuses its activity on an in-depth exploration of the cellular and molecular mechanisms governing the development, plasticity, aging, and pathophysiology of the nervous system. Particular attention is devoted to Duchenne Muscular Dystrophy, a condition traditionally considered muscular but now recognized for its significant implications on both the central and peripheral nervous systems, with consequences for neurodevelopment, cognitive functions, and multiple neurobiological processes.

We are interested in intraspecific diversity of insects, mainly phytophagous and saproxylic species, in both evolutionary contexts—concerning insect–plant relationships and the adaptive significance of genetic polymorphisms in groups of phytophagous beetles (mainly Weevils and Leaf Beetles)—and in conservation-related issues, particularly in the prioritization of protected areas aimed at safeguarding insect species included in the Habitats Directive.

Research in my laboratory is characterized by a multidisciplinary and multiscale approach. We combine behavioural, anatomical, molecular and bioinformatics analyses with chemogenetic or optogenetic manipulations of neural activity, with the aim to build a comprehensive understanding of neural circuits in both normal and pathological conditions.

Our research investigates the mechanisms underlying cellular recovery, with a particular emphasis on the role of nutrients as active modulators of repair and adaptation processes, especially in neural models exposed to oxidative stress or harboring rare metabolic mutations. We study how micronutrients—at both physiological and pharmacological doses—affect neural-like cells, focusing on metabolism as a potential upstream modulator rather than a downstream consequence.

We study a group of protein conformational diseases caused by polymerisation of mutant serpins (serin proteinase inhibitors), specifically the neuronal protein neuroserpin and the hepatic serpin alpha-1 antitrypsin. The mechanism of inhibition of serpins requires a high molecular flexibility that renders them very sensitive to destabilising mutations.