Clear differences in the clinical course of C. trachomatis infections in women have been observed, which are not explained by bacterial factors. This suggests that there might be differences in the host genetic background associated with the recognition of pathogens and the immune response that ensues. Indeed, recent research indicates the relevance for studying the host genetic background in relation to disease susceptibility. In one study, an analysis of the lymphoproliferative responses to C. trachomatis antigen among Gambian monozygotic versus dizygotic twins in a trachoma endemic region indicated an almost 40% contribution of heritability to the observed differences in the response. Duchenne muscular dystrophy is a genetic disorder characterized by absence of the cytoskeletal protein dystrophin. This is RAD001 recapitulated in the DMD mouse model. Absence of dystrophin leads to loss of anchoring of the myofiber to the basal lamina, eliciting subsequent myofiber degeneration that in turn results in progressive loss of muscle mass, weakness, and increased extracellular matrix accumulation. Thus, children with this pathology gradually and progressively lose muscle strength, typically requiring the use of a wheelchair from the age of 10 and dying in the late second or early third decade of life as a result of cardiorespiratory arrest. Pathologic features of DMD include myofiber atrophy, fatty accumulation, 
degeneration, necrosis, and fibrosis, which dramatically affect the environment of the fibers and normal muscle physiology. Fibrosis is a complex and incompletely Epoxomicin understood process characterized by excessive accumulation of collagens and other ECM components. It occurs under chronic disease conditions and affects various tissues and organs. Several findings support the notion that fibrosis directly contributes to progressive muscle dysfunction and the lethal phenotype of DMD. Targeting the renin-angiotensin system is one of the most common therapeutic approaches in cardiovascular medicine. Traditional pharmacologic RAS intervention seeks to prevent excessive AT1 receptor stimulation by repressing synthesis of angiotensin II through inhibition of renin or angiotensinconverting enzyme or by direct blockade of the AT1 receptor. This strategy has been successful in cardiovascular therapy, as documented by numerous clinical studies demonstrating reduced mortality and morbidity in treated patients. In recent years other receptors of the RAS have been better characterized in terms of signaling and physiologic function, revealing the existence of a so-called ”alternative” or ”protective” RAS including AT2 and Mas receptor. These receptors mediate tissue protective activities that counteract not only the AT1 receptor, but also inflammatory cytokines, growth factors, and proapoptotic stimuli. Stimulation of AT2 receptor or Mas has been shown to ameliorate the course of cardiovascular, renal, immunological, and neurological diseases in multiple experimental models. Thus, AT2 receptors and Mas are now regarded as potential drug targets, and respective agonists are in various phases of drug development. Angiotensin-1-7 ) is an endogenous bioactive peptide metabolite in the alternative or protective arm of RAS. It is primarily derived from angiotensin II processing and has important biological effects including vasodilation, inhibition of cell proliferation.