Hematopoietic colony stimulating factors in cardiovascular and pulmonary remodeling: promoters or inhibitors?
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.
Parissis
John
J
2nd Department of Cardiology, University of Athens, Atticon University Hospital, Rimini 1, 12461, Athens, Greece.
Filippatos
Gerasimos
G
Adamopoulos
Stamatis
S
Li
Xiaopeng
X
Kremastinos
Dimitrios Th
DT
Uhal
Bruce D
BD
D000818:Animals; D003115:Colony-Stimulating Factors / Q000009:adverse effects / Q000502:physiology* / Q000627:therapeutic use; D004305:Dose-Response Relationship, Drug; D006801:Humans; D008168:Lung / Q000187:drug effects / Q000473:pathology; D011658:Pulmonary Fibrosis / Q000139:chemically induced / Q000503:physiopathology*; D020257:Ventricular Remodeling / Q000187:drug effects / Q000502:physiology*
D003115:Colony-Stimulating Factors