MEK-inhibitors decrease Nfix in muscular dystrophy but induce unexpected calcifications, partially rescued with Cyanidin diet.

Muscular dystrophies (MDs) are incurable genetic myopathies characterized by progressive degeneration of skeletal muscles. Dystrophic mice lacking the transcription factor Nfix display morphological and functional improvements of the disease. Recently, we demonstrated that MAPK signaling pathway positively regulates Nfix in muscle development and that Cyanidin, a natural antioxidant molecule, strongly ameliorates the pathology.

Adipose tissue regeneration: a state of the art.

Adipose tissue pathologies and defects have always represented a reconstructive challenge for plastic surgeons. In more recent years, several allogenic and alloplastic materials have been developed and used as fillers for soft tissue defects. However, their clinical use has been limited by further documented complications, such as foreign-body reactions potentially affecting function, degradation over time, and the risk for immunogenicity.

Potential for neural differentiation of mesenchymal stem cells.

Adult human stem cells have gained progressive interest as a promising source of autologous cells to be used as therapeutic vehicles. Particularly, mesenchymal stem cells (MSCs) represent a great tool in regenerative medicine because of their ability to differentiate into a variety of specialized cells. Among adult tissues in which MSCs are resident, adipose tissue has shown clear advantages over other sources of MSCs (ease of surgical access, availability, and isolation), making adipose tissue the ideal large-scale source for research on clinical applications.

Synaptic dysfunction in Alzheimer's disease.

Generation of amyloid peptide (Aβ) is at the beginning of a cascade that leads to Alzheimer's disease (AD). Amyloid precursor protein (APP), as well as β- and γ-secretases, is the principal player involved in Aβ production, while α-secretase cleavage on APP prevents Aβ deposition. Recent studies suggested that soluble assembly states of Aβ peptides can cause cognitive problems by disrupting synaptic function in the absence of significant neurodegeneration.

Alpha, beta-and gamma-secretases in Alzheimer's disease.

Generation of Amyloid peptide (Abeta) is at the beginning of a cascade that leads to Alzheimer's disease. Currenty, the mechanisms of Abeta generation and Abeta prevention are subject of intensive research. Amyloid precursor protein (APP), as well as beta- and gamma-secretases are the principal players involved in Abeta production, while alpha-secretase cleavage on APP prevents Abeta deposition.