The LMNA G608G transgenic mice targeted the expression of the Nutlin-3 Hutchinson-Gilford progeria syndrome mutation in keratin-5-expressing tissue led to a typical phenotype of HGPS. LMNA H222P mutated gene knockin mice exhibited conduction defects, chamber dilation, increased fibrosis and lack of hypertrophy, and also showed muscular dystrophy and death at 4–9 months of age. The patients with heterozygous for the LMNA E82K mutation showed clinical phenotypes of heart dilation and associated with conduction system disease at their onset age of 32 or 33 years. The two LmnaE82K transgenic mice lines exhibited chamber dilation, increased heart weights, increased fibrosis, upregulation of hypertrophic maker expression, nuclear structure defects and conduction defects, which was similar with the phenotypes of the patients carrying the LMNA E82K mutation. The importance of BNP as a diagnostic and therapeutic modality in cardiovascular disease is well known, it also acts as a local regulator of ventricular remodeling and a modifier of cardiac gene expression. Acta1 is present in the developing heart and it constitutes up to 20% of the striated actin of the adult heart. Since Acta1 is a multifunctional protein that interacts with many proteins involved in folding, polymerisation, contractility and regulation of contractility, abnormal levels may affect any of those functions. In the normal adult heart, approximately 2 to 4% of the myocardium is made up of collagen. The Col3a1 is one of the essential components of the cardiovascular extracellular matrix, maintaining structural and functional integrity of myocardium and thought to be responsible for abnormal myocardial stiffness and for the impaired pumping capacity of the heart. LMNA E82K mutation located in the coil 1B domain of central a helical rod domain of the lamin A and the lamin C proteins, those were conserved regions of the rod domain which have been shown to play crucial roles in the assembly of intermediate filament dimers into higher order oligomers. Mutations affect this region of IF proteins and may disrupt the interaction between the monomers and are linked to several diseases. Members of the intermediate filament superfamily are critical mechanical integrators of the nuclear membrane and the cytoskeleton, protecting the cell from repeated mechanical stress. Mutations in the lamin A/C gene may cause cardiomyopathy by weakening nuclei, which increase the fragility of nuclei and could be particularly harmful to muscle cells. Forces generated during muscle contraction might potentially lead to preferential breakage of nuclei containing a defective nuclear lamina.