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Updated: Aug 9, 2026
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Published on: March 30, 2022
G-CSF administration after myocardial infarction in mice attenuates late ischemic cardiomyopathy by enhanced
Elisabeth Deindl1, Marc-Michael Zaruba, Stefan Brunner
1Ludwig-Maximilians University, Klinikum Grosshadern, Medical Department I, Marchioninistr. 15, D-81377 Munich, Germany.
Insights
Granulocyte-colony stimulating factor (G-CSF) enhances blood vessel growth and improves heart function after myocardial infarction (MI). This G-CSF treatment reduces scar tissue and increases survival rates in mice.
Area of Science:
- Cardiovascular Biology
- Regenerative Medicine
- Hematology
Background:
- Granulocyte-colony stimulating factor (G-CSF) improves cardiac function post-myocardial infarction (MI) via cell mobilization and cardiomyocyte protection.
- The role of G-CSF in collateral artery growth (arteriogenesis) after MI remains unclear.
Purpose of the Study:
- To investigate the effect of G-CSF on arteriolar growth and cardiac function in a murine MI model.
Main Methods:
- Mice received G-CSF (100 microg/kg/day) for 5 days post-MI.
- Assessed circulating mononuclear cells, arteriolar ICAM-1 expression, cell proliferation, histology, survival rates, and cardiac function (pressure-volume loops).
Main Results:
- G-CSF increased circulating stem cell markers and promoted arteriolar growth with bone marrow cell accumulation in the infarct border zone.
- Reduced granulation tissue, LV wall thinning, and scar extension were observed.
- G-CSF significantly improved post-MI survival and partially restored myocardial function (EF: 32.5% vs. 17.2% at day 30).
Conclusions:
- G-CSF administration post-MI stimulates arteriogenesis.
- G-CSF treatment attenuates ischemic cardiomyopathy and improves cardiac outcomes after myocardial infarction.
Abstract:
Granulocyte-colony stimulating factor (G-CSF) has been shown to improve cardiac function after myocardial infarction (MI) by bone marrow cell mobilization and by protecting cardiomyocytes from apoptotic cell death. However, its role in collateral artery growth (arteriogenesis) has not been elucidated. Here, we investigated the effect of G-CSF on arteriolar growth and cardiac function in a murine MI model. Mice were treated with G-CSF (100 microg/kg/day) directly after MI for 5 consecutive days. G-CSF application resulted in a significant increase of circulating mononuclear cells expressing stem cell markers. Arterioles in the border zone of infarcted myocardium showed an increased expression of ICAM-1 accompanied by an accumulation of bone marrow derived cells and a pronounced proliferation of endothelial and smooth muscle cells. Histology of G-CSF treated mice revealed a lower amount of granulation tissue (67.8 vs. 84.4%) associated with a subsequent reduction in free LV wall thinning and scar extension (23.1 vs. 30.8% of LV). Furthermore, G-CSF treated animals showed a significant improvement of post-MI survival (68.8 vs. 46.2%). Pressure-volume relations revealed a partially restored myocardial function at day 30 (EF: 32.5 vs. 17.2%). Our results demonstrate that G-CSF administration after MI stimulates arteriogenesis and attenuates ischemic cardiomyopathy after MI.
