Norma L. Gómez-Viquez

TL;DR: The maturation of ECC in the rat heart during postnatal development is investigated and the first well-integrated information that links the developing organization of proteins underlying EC coupling (RyR2, DHPR, Cav3 and JP2) to the developing efficacy of EC coupling is provided.

TL;DR: The results suggest that nuclear Ca(2+) levels underlie the regulation of specific protein targets and thereby modulate cardiomyocyte function.

TL;DR: Test the hypothesis that decreased SERCA2a activity is mediated by elevated oxidative stress produced in the MetS heart and myocytes from MetS rats treated with the antioxidant N-acetylcysteine showed normal ROS levels and SERCA 2a-mediated Ca(2+) reuptake as well as accelerated cytosolic Ca( 2+) removal, and suggest that elevated oxidative Stress may induce oxidative modifications on SER CA2a leading to abnormal function of this protein in the metS heart.

TL;DR: The role of Ca(2+) mishandling in the development of cardiac dysfunction in obesity and IR is focused on and the evidence suggesting that OS might also contribute to cardiac dysfunction by affecting Ca( 2+) handling is addressed.

TL;DR: It is concluded that decreased SR Ca2+, due to slower SERCA, disrupts systolic RyR2 synchronization, and this underlies Ca2+ and contractility dysregulation.