Skip to main content
. Author manuscript; available in PMC: 2020 Jul 2.
Published in final edited form as: Circulation. 2019 Apr 15;140(1):55–66. doi: 10.1161/CIRCULATIONAHA.119.039751

Figure 7. Model for NEXN role in cardiomyocytes.

Figure 7.

At prenatal stage, NEXN is essential for the establishment of the JMCs. During neonatal stage (around P5), NEXN stabilization of the JMC allow the PM/SR tethering and PM buds start to invaginate inside the cell. Later in the development (around P10), the proper formation of JMCs leads to the deeper invagination of the forming T-tubules and the maturation of the dyads. Indeed, in cardiomyocytes lacking NEXN, the decrease of 12nm gap size junctions is observed. Furthermore, absence of NEXN prevent the sarcolemmal invaginations at P5 followed by a non-formation of T-tubules at P10. Finally, as a result of the altered membrane network, loss of NEXN in cardiomyocytes induce EC-coupling defects accompanied by severe DCM.