Our study shows that the progeria c.1824C > T (p.Gly608Gly) mutationcaused a decrease in cell adhesion and relaxation time propertiesin cardiomyocytes that may lead to the impairment of force production.Furthermore, we found altered frequency and rhythm of spontaneousbeating and calcium handling in a single-cardiomyocyte cell model,along with a decrease in Cx43 localization, suggesting that disruptedmechanotransduction and mechanosignaling lead to electrophysiologicaldysfunction in HGPS cardiomyocytes. This evidence concerns the gene GJA1 and progeroid syndrome.