Targeting the myocardial XXXX - @entity3884 exchange for treatment of @entity712 .

@entity32815 @entity712 @entity3884 @entity5721 @entity296 @entity2232 @entity1184 @entity2178 @entity1372 @entity1188 @entity44185
Although the past number of years have seen a substantial improvement in the therapeutic approaches for the treatment of @entity712 , mortality rates continue to be high. Moreover, the incidence of @entity712 is expanding rapidly. @entity1372 - @entity3884 exchange ( @entity44185 ) is a key target for the treatment of @entity712 . @entity44185 is a major mechanism for intracellular pH regulation in most cell types, including the cardiac cell. Seven isoforms of @entity44185 have been identified so far although cardiac cells possess primarily the ubiquitous @entity32815 subtype. @entity32815 is a major contributor to @entity5721 and @entity32815 inhibitors exert marked cardioprotective effects, particularly when administered before ischaemia, findings which have now been extended to clinical trials. It is emerging that @entity32815 also contributes to chronic maladaptive myocardial responses to injury ( @entity296 ) and may contribute to the development of @entity712 . Experimental studies using both in vitro approaches as well as animal models of @entity712 have consistently demonstrated a beneficial effect of @entity32815 inhibitors in terms of inhibition of @entity1184 in response to various stimuli as well as inhibiting @entity712 after coronary artery ligation. These effects occurred independently of any @entity1188 size reducing effects of @entity32815 inhibitors or on any direct effects on afterload thus indicating a direct effect on the @entity296 process. In fact, it appears that @entity32815 may represent a common downstream mediator for various hypertropic factors such as @entity2178 , @entity2232 and beta(1) adrenergic receptor activation. @entity32815 inhibition, therefore, represents a potentially effective new therapeutic approach for the treatment of @entity712 .
