By Frank I. Marcus, Andrea Nava, Gaetano Thiene
This e-book covers all facets (biological, pathological, genetics, scientific and therapeutical) of arrhythmogenic correct ventricular cardiomyopathy/dysplasia, a contemporary cardiomyopathy which represents a truly excessive probability of unexpected loss of life within the younger and in athletes. The monograph provides the result of 5-year examine software on ARVC/D supported by way of delivers of either the ecu fee and the NIH, which enabled the invention of seven disease-causing genes, hence beginning new avenues for the early identity of affected sufferers and for unexpected dying prevention. A panel of best scientists, either eu and americans, contributed to this quantity, that allows you to be a necessary reference for pros and citizens in cardiology, radiology, human genetics, and recreation medication.
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Extra info for Arrhythmogenic right ventricular cardiomyopathy dysplasia: Recent Advances
Varga J, Jimenez SA (1986) Stimulation of normal human fibroblast collagen production and processing by transforming growth factor-beta. Biochem Biophys Res Commun 138:974-980 28 Barbara Bauce, Andrea Nava 27. Overall CM, Wrana JL, Sodek J (1989) Independent regulation of collagenase, 72-kDa progelatinase, and metalloendoproteinase inhibitor expression in human fibroblasts by transforming growth factor-beta. J Biol Chem 264:1860-1869 28. Kirchhof P, Fabritz L, Zwiener M et al (2006) Age- and training-dependent development of arrhythmogenic right ventricular cardiomyopathy in heterozygous plakoglobin-deficient mice.
Recently, Garcia Gras et al. , reported their findings with heterozygous desmoplakin-deficient mice. They showed excess adipocytes and fibrosis in the myocardium, increased myocyte apoptosis, cardiac dysfunction, and ventricular arrhythmias, mimicking the phenotype of human fibro-fatty ARVC/D. The authors provided evidence that expression and nuclear localization of PPAR-γ, a major regulator of adipogenesis, was restricted to fibrotic areas in desmoplakin-deficient mouse hearts, suggesting a possible origin of adipocytes from fibrocytes or prefibroblasts, which are considered adipocyte progenitor cells, rather than cardiac myoblasts or resident and circulating mesenchymal stem cells.
Bauce B, Nava A, Rampazzo A et al (2000) Familial effort polymorphic ventricular arrhythmias in apparently normal heart map to chromosome 1q42-q43. Am J Cardiol 85:573-579 14. Bauce B, Rampazzo A, Basso C et al (2002) Screening for RyR2 mutations in families with effort-induced polymorphic ventricular arrhythmias and sudden death: Early diagnosis of asymptomatic carrier. J Am Coll Cardiol 40:341-349 15. Priori S, Napolitano C, Tiso N et al (2001) Mutations in the cardiac ryanodine receptor gene (hRyR2) underlie catecholaminergic polymorphic ventricular tachycardia.