2005
DOI: 10.1016/j.ijcard.2004.08.053
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Functional improvement in heart failure patients treated with beta-blockers is associated with a decline of cytokine levels

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Cited by 49 publications
(34 citation statements)
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“…The present findings are consistent with previous data showing that myeloid lineage immune cells and their innate effector molecules, such as proinflammatory cytokines and type I interferons, are regulated by β-adrenergic signaling (7,(57)(58)(59)(60)(61)(62) and adverse socioenvironmental conditions (2,7,10,13,17,63). These results are also consistent with previous findings that nonsocial activators of β-adrenergic signaling, such as burn-induced sepsis, can enhance monocyte differentiation (28,29).…”
Section: Discussionsupporting
confidence: 93%
“…The present findings are consistent with previous data showing that myeloid lineage immune cells and their innate effector molecules, such as proinflammatory cytokines and type I interferons, are regulated by β-adrenergic signaling (7,(57)(58)(59)(60)(61)(62) and adverse socioenvironmental conditions (2,7,10,13,17,63). These results are also consistent with previous findings that nonsocial activators of β-adrenergic signaling, such as burn-induced sepsis, can enhance monocyte differentiation (28,29).…”
Section: Discussionsupporting
confidence: 93%
“…It has been shown previously that an increase in CDS activity was associated with increased secretion of the pro-infl ammatory mediators, tumor necrosis factor-␣ , and interleukin-6, from ECV304 cells upon stimulation with interleukin-1 ␤ ( 36 ). An increase in tumor necrosis factor-␣ and interleukin-6 content has been observed in SHHF rats at 15 months of age ( 12 ), indicating that increased CDS activity as observed in the present study may be related to the increased secretion of these infl ammatory mediators, which are known to cause contractile dysfunction ( 37 ). However, further studies are needed to fi nd a direct relationship between contractile dysfunction, CDS activity, and release of pro-infl ammatory mediators at compensated and terminal stages of HF in SHHF rats.…”
Section: Discussionsupporting
confidence: 71%
“…Like was seen in our results, HF group had higher baseline IL-6 levels 38 , but we didn't observe at rest hypoxic response. We didn't find other studies with HF and hypoxic IL-6 answer, but it was described that beta-blockers use repressed IL-6 response even in pathologic situations 39 . So, we hypothesized that in our study at rest in HF group IL-6 response could be inhibited by beta-blocker action still that hypoxic stimulus.…”
Section: Catecholamines Bnp Aldosterone Nitric Oxide and Interleukmentioning
confidence: 91%