Enrique Brandan

Investigación

Muscular Fibrosis

Fibrosis is the natural consequence of tissue repair and aging, but is also promoted by diverse diseases and can have a genetic component, as epitomized by Duchenne muscle dystrophy (DMD). The fibrotic disorders  are characterized by an excessive scar tissue accumulation, that replacing the normal tissue, causes the malfunctioning of tissues and organs. A predominant compromise of heart, lung, kidney or skeletal muscle usually cause severe health weaknesses. Present treatments are ineffective, mainly because their lack in target specificity. Expect to disclose new approaches to preclude pathogenic fibrosis in general, applicable to other organs and situations. The approaches include "upstream" mechanisms dealing with the production of factors that modulate fibrosis and "downstream" mechanisms regulating intracellular signaling. From the experimental approaches to skeletal muscle and renal fibrosis, crossed experiments will be done to disclose the common mechanisms that might be involved. Thus, the antifibrotic hormones that are effective in the kidney will be use in the models of muscle fibrosis and vice-versa.

Objetivs:

• Skeletal muscle differentiation
• Skeletal muscle regeneration and fibrosis Role of CTGF