Energy Production and Utilization in Contractile Failure Due to Intracellular Calcium Overload

MAPK activation and apoptotic alterations in hearts subjected to calcium paradox are attenuated by taurine

“…In this regard, Takahasi et al [40] have also shown an elevation of Bcl-2 protein content by taurine as this was considered to render the cell resistant to ischemiamediated injury. Our previous study has shown that mitochondrial respiration and oxidative phosphorylation rate was significantly depressed in mitochondria isolated from Ca 2+ -paradoxic hearts [41]. Although in the present study we have not examined the effect of taurine on the status of mitochondrial membrane potential and cytochrome c release, no effect of taurine on these parameters was observed in a model of simulated ischemia [13].…”

Role of intracellular Ca2+ overload in inducing changes in cardiac gene expression

“…This view is supported by the fact that a marked cardiac contracture was demonstrated to be intimately associated with a marked increase in the intracellular Ca 2+ content in the CP heart (16). Varying degrees of alterations in functional and biochemical activities of SL, SR and MF activities have also been shown to occur in CP hearts as a consequence of intracellular Ca 2+ overload (13)(14)(15)17,(21)(22)(23). Although elevated levels of intracellular Ca 2+ have been observed to activate proteases, such as calpains, directly the observed increase in mRNA levels for both calpain-1 and -2 proteins may also contribute to increased calpain activity in hearts under different pathological conditions associated with the occurrence of intracellular Ca 2+ overload (27)(28)(29)(30)(31).…”

“…We have reported that the inability of CP hearts to recover contractile function was associated with a marked increase in intracellular Ca 2+ , as well as the development of cardiac contracture, ultrastructural damage and subcellular defects (11,13,15,16,21,23). In the present study, we examined whether hearts perfused with Ca 2+ -free medium followed by reperfusion with medium containing different concentrations of Ca 2+ exhibit alterations in gene expression for SL Na + -K + ATPase and Na + -Ca 2+ exchanger, SR Ca 2+ -pump ATPase, Ca 2+ -release channel and phospholamban (PLB), as well as MF α-and β-myosin heavy chain proteins.…”

“…Accordingly, it has been suggested that cardiac dysfunction in failing hearts is due to subcellular remodelling as a consequence of changes in cardiac gene expression (2,(7)(8)(9). Although the occurrence of intracellular Ca 2+ overload is believed to be intimately involved in the genesis of cardiac dysfunction in heart failure (10)(11)(12)(13)(14)(15), its role in inducing defects in cardiac gene expression is not fully understood. It was, therefore, the purpose of the present study to investigate whether alterations in gene expression of SL, SR and MF proteins occur during the development of intracellular Ca 2+ overload in the myocardium.…”

High-Energy Phosphates and Ischemic Heart Disease: From Bench to Bedside

“…Several studies have shown that intracellular Ca 2+ overload is a major cause of myocardial cell damage and cardiac dysfunction in IHD. CrP can reduce Ca 2+ influx by providing energy to ATP-dependent Ca 2+ ATPase and Na + -K + ATPase on the plasma membrane ( 102 , 103 ). At the same time, the Ca 2+ ATPase activity on the sarcoplasmic reticulum is restored, and Ca 2+ enter the sarcoplasmic reticulum to avoid the myocardial stiffness contracture ( 104 ).…”