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- W2325101359 abstract "Background: Myocardial infarction is a leading cause of mortality worldwide. Over the last decade, a novel approach of regenerative cell therapy arose with the aim to improve cardiac repair by using stem/progenitor cells. The chemokine CXCL12/SDF-1 has been described as a key player in this process by recruiting inflammatory and stem cells to the site of injury. Most studies using pharmacological targeting of SDF-1 and gain-of-function experiments revealed a beneficial effect of the chemokine on cardiac remodeling. Results: In order to further clarify its role in cardiac repair, we generated conditional knockout (cKO) mice lacking SDF-1 specifically in cardiomyocytes. These mice revealed normal cardiac structure and function at basal levels, but they proved to be resistant to cardiac hypertrophy and fibrosis when subjected to angiotensin II infusion. Furthermore, the induction of myocardial infarction resulted in reduced scar size and decreased infiltration of macrophages in cKO mice compared to controls. In addition, we generated transgenic (Tg) rats overexpressing SDF-1 exclusively in cardiomyocytes. Upon induction of myocardial infarction, these animals showed a worsened cardiac function accompanied by more fibrosis development in comparison to controls, thus supporting our findings in cKO mice. Conclusion: In summary, SDF-1 seems to play an important role in cardiac hypertrophy, fibrosis, and peri-infarction inflammation. Myocardial infarction experiments in both SDF-1 cKO mice and Tg rats reveal a detrimental effect of cardiomyocyte-derived SDF-1 due to paracrine effects in the heart and/or recruitment of inflammatory cells. These features should cause caution when targeting SDF-1 in clinical applications." @default.
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- W2325101359 date "2012-09-01" @default.
- W2325101359 modified "2023-09-24" @default.
- W2325101359 title "805 THE DARK SIDE OF CARDIOMYOCYTE-SPECIFIC CXCL12/SDF-1" @default.
- W2325101359 doi "https://doi.org/10.1097/01.hjh.0000420836.17085.67" @default.
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