Ricerc@Sapienza

The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway is a key intracellular mediator of a variety of metabolically relevant hormones and cytokines, including the interleukin-6 (IL-6) family of cytokines. The JAK/STAT pathway transmits extracellular signals to the nucleus, leading to the transcription of genes involved in multiple pleiotropic biological activities. The JAK/STAT pathway has been reported to be required for the homeostasis of different tissues and organs, where it is required for normal homeostasis.

Background: Histone deacetylase 4 (HDAC4) has been proposed as a target for Amyotrophic Lateral Sclerosis (ALS) because it mediates nerve-skeletal muscle interaction and since its expression in skeletal muscle correlates with the severity of the disease. However, our recent studies on the skeletal muscle response upon long-term denervation highlighted the importance of HDAC4 in maintaining muscle integrity. Methods: To fully identify the yet uncharacterized HDAC4 functions in ALS, we genetically deleted HDAC4 in skeletal muscles of a mouse model of ALS.

Background: The effect of gene polymorphisms and promoter methylation, associated with maladaptive developmental outcomes, vary depending on environmental factors (e.g., parental psychopathology). Most studies have focused on 0- to 5-year-old children, adolescents, or adults, whereas there is dearth of research on school-age youths and pre-adolescents.

Aims Metabolic cardiomyopathy (MC)-characterized by intra-myocardial triglyceride (TG) accumulation and lipotoxic damage-is an emerging cause of heart failure in obese patients. Yet, its mechanisms remain poorly understood. The Activator Protein 1 (AP-1) member JunD was recently identified as a key modulator of hepatic lipid metabolism in obese mice. The present study investigates the role of JunD in obesity-induced MC.

There is growing research interest for the role of genetic and epigenetic factors in the etiopathogenesis of Hashimoto's Thyroiditis (HT).
HT is an organ-specific autoimmune thyroid disease (AITD) accounting for most cases of clinical hypothyroidism and in which both cellular and humoral immunity have a role in the pathogenesis. HT is characterized by diffuse goiter supported by thyroid-specific autoantibodies and

In this brief review, we present evidence of the primary role of learning-associated plasticity in the development of either adaptive or maladaptive coping strategies.

Oxidative stress (OS) is associated with many diseases ranging from cancer to neurodegenerative disorders. Nuclear factor-erythroid 2 p45-related factor 2 (Nrf2) is one of the most effective cytoprotective controller against OS. Modulation of Nrf2 pathway constitutes a remarkable strategy in the antineoplastic treatments. A big number of Nrf2-antioxidant response element activators have been screened for use as chemo-preventive drugs in OS associated diseases like cancer even though activation of Nrf2 happens in a variety of cancers.

Skeletal muscle possesses a remarkable capacity to regenerate upon injury thanks to the presence of a population of stem cells called muscle satellite cells (MuSCs). These cells, normally quiescent in resting conditions, become activated by extracellular cues released in the regenerative environment, expand and then differentiate into mature myofibers to properly repair injured muscles. During regenerative cycles, MuSCs undergo dramatic epigenetic changes that dictate activation or repression of specific transcriptional programs needed to transit along different cell fates.

Many studies have consistently demonstrated an epigenetic link between environmental stimuli and physiological as well as cognitive responses. Epigenetic mechanisms represent a way to regulate gene activity in real time without modifying the DNA sequence, thus allowing the genome to adapt its functions to changing environmental contexts. Factors such as lifestyle, behavior, and the practice of sitting and moving mindful activities have been shown to be important means of environmental enrichment.

Adult neurogenesis declines with aging due to the depletion and functional impairment of neural stem/progenitor cells (NSPCs). An improved understanding of the underlying mechanisms that drive age-associated neurogenic deficiency could lead to the development of strategies to alleviate cognitive impairment and facilitate neuroregeneration. An essential step towards this aim is to investigate the molecular changes that occur in NSPC aging on a genomewide scale.