Effects of G-CSF on left ventricular remodeling and heart failure after acute myocardial infarction View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2006-01-17

AUTHORS

Hiroyuki Takano, Yingjie Qin, Hiroshi Hasegawa, Kazutaka Ueda, Yuriko Niitsuma, Masashi Ohtsuka, Issei Komuro

ABSTRACT

Granulocyte colony-stimulating factor (G-CSF) is a hematopoietic cytokine that promotes proliferation and differentiation of neutrophil progenitors. G-CSF also possesses immunomodulatory properties. G-CSF-induced hematopoietic stem cell mobilization is widely used clinically for transplantation. After it was recently reported that G-CSF mobilizes bone marrow stem cells (BMSCs) into the infarcted hearts and accelerates the differentiation into vascular cells and cardiac myocytes, myocardial regeneration utilizing mobilization of BMSCs by G-CSF is attracting the attention of investigators. In animal models, G-CSF prevents left ventricular remodeling and dysfunction after acute myocardial infarction, at least in part, through a decrease in apoptotic cells and an increase in vascular cells. Although it is controversial whether BMSCs mobilized by G-CSF can differentiate into cardiac myocytes, G-CSF-induced angiogenesis is indeed recognized in infarcted heart. The cardioprotective effects of G-CSF are recognized even in isolated perfused heart. In addition, G-CSF activates various signaling pathways such as Akt, extracellular signal-regulated kinase, and Janus kinase 2/signal transducer and activator of transcription 3 through G-CSF receptors in cardiac myocytes. These observations suggest that G-CSF not only induces mobilization of stem cells and progenitor cells but also acts directly on cardiomyocytes. Therefore, G-CSF may be utilized as a novel agent to have protective and regenerative effects on injured myocardium. Although the effects of G-CSF on the progression of atherosclerosis are still unclear, there is a possibility that G-CSF will become a promising therapy for ischemic heart diseases. More... »

PAGES

185-193

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00109-005-0035-z

DOI

http://dx.doi.org/10.1007/s00109-005-0035-z

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1010236760

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/16418824


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