Clinical and neurohormonal correlates of circulating granulocyte-macrophage colony-stimulating factor in severe heart failure secondary to ischemic or idiopathic dilated cardiomyopathy

Parissis, John; Adamopoulos, Stamatis; Venetsanou, Koula; Mentzikof, D.; Karas, S.; Kremastinos, Dimitrios Th.

doi:10.1016/s0002-9149(00)01062-6

Cited by 21 publications

(14 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, these inhibitory effects correlated perfectly with the results obtained in the cytokine protein expression assays using a mouse cytokine protein array. Several studies have shown that plasma M-CSF concentrations are raised in patients with severe unstable angina [40], and severe heart failure [41]. Furthermore, t-RESV has been reported to inhibit basal release of GM-CSF by alveolar macrophages [42].…”

Section: Discussionmentioning

confidence: 99%

Effect of cis-resveratrol on genes involved in nuclear factor kappa B signaling

Leiro

Arranz

Fraiz

et al. 2005

International Immunopharmacology

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Effect of cis-resveratrol on genes involved in nuclear factor kappa B signaling

Leiro

Arranz

Fraiz

et al. 2005

International Immunopharmacology

View full text Add to dashboard Cite

“…1) [21,22,64]. Parissis et al [22] found that one month after the onset of acute myocardial infarction, enhanced GM-CSF activation is present in patients with severe left ventricular dysfunction, and is significantly correlated with increased left ventricular dimensions.…”

Section: Gm-csfmentioning

confidence: 99%

“…Furthermore, enhanced peripheral monocytosis, monocyte recruitment into the infarcted myocardium and delayed collagen production by GM-CSF induction may lead to infarct expansion and aggravated LV remodeling and dysfunction [67]. Recently, we have reported that plasma GM-CSF levels were elevated in patients with ischemic dilated cardiomyopathy and that this increase was associated with the degree of LV dysfunction and neurohormonal activation [21]. Another study demonstrated that GM-CSF administration in cancer patients reduced cardiac contractility [68].…”

Section: Gm-csfmentioning

confidence: 99%

“…Because of their proliferative effects on hematopoietic cells, some of these recombinant proteins were introduced into clinical trials to evaluate medical benefits in various hematological disorders [15,16]. On the other hand, recent experimental and clinical data suggest that HCSFs are actively implicated in the pathophysiology of several cardiovascular disorders, such as vascular remodeling, atherosclerosis, arterial hypertension, acute coronary syndromes, ischemia/reperfusion injury, post-infarction left ventricular remodeling, chronic heart failure [17][18][19][20][21][22] and in pulmonary fibrosis . In this article, we review the pathophysiologic role of HCSFs in the development and progression of cardiovascular disease and lung fibrosis, and discuss the potential role of HCSF-mediated therapy in pathological tissue remodeling.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Hematopoietic Colony Stimulating Factors in Cardiovascular and Pulmonary Remodeling: Promoters or Inhibitors?

Parissis

Filippatos²,

Adamopoulos

et al. 2006

CPD

Self Cite

View full text Add to dashboard Cite

Hemopoietic colony stimulating factors (HCSFs) are naturally occurred substances that are released in response to infection or inflammation and regulate the proliferation and differentiation of hemopoietic progenitor cells. Some representative members of this peptide family induce atherogenesis through the mediation of monocyte-endothelial cell adhesive interaction and promotion of angiogenesis within the atherosclerotic plaques. HCSFs, such as granulocyte-macrophage colony-stimulating factor (GM-CSF), also promote post-infarction cardiac remodeling though the enhanced activation and infiltration of monocytes into injured myocardial tissue and through altered equilibrium of collagen deposition/degradation. On the other hand, exogenous administration of granulocyte colony-stimulating factor (G-CSF) or eythropoietin (EPO) in patients with chronic ischemic disease or recent myocardial infarction have lead to beneficial arteriogenesis or myocardial cell regeneration, thus preventing adverse cardiac remodeling. While GM-CSF may hold therapeutic potential as an inhibitor of lung fibrogenesis, G-CSF appears to promote fibrosis in the lungs. The pathophysiological role of HCSFs also depends on the timing of their action on cardiovascular remodeling, as well as on the target progenitor hematopoietic cell. This article summarizes current knowledge about the clinical and therapeutic implications of these factors in chronic artery disease, post-infarction cardiac remodeling, chronic heart failure and in pulmonary fibrosis.

show abstract

“…It has been reported that peripheral monocytosis is associated with LV remodeling after MI (4). Another study demonstrated that plasma GM-CSF levels were elevated in patients with ischemic dilated cardiomyopathy and that this increase was associated with the degree of LV dysfunction (5). Romurtide, which is a synthetic muramyldipeptide derivative, has been known to act as a GM-CSF inducer by binding to monocytes and macrophages (6,7).…”

mentioning

confidence: 99%