Proinflammatory cytokine expression in the adult mammalian heart is regulated by both load-dependent and load-independent mechanisms during hemodynamic overloading.
Sustained hemodynamic overloading provokes a transient increase in proinflammatory cytokine and cytokine receptor gene expression; however, the decrease in proinflammatory cytokine gene expression occurred in the absence of changes in loading conditions, suggesting that the expression of proinflammatory cytokines in the heart is regulated, at least in part, by load-dependent and load-independent mechanisms.
Baumgarten et al. (Tue,) studied this question.