Why the study?
Does the bispecific SDF1-GPVI fusion protein improve myocardial repair and preserve cardiac function in a mouse model of myocardial infarction?
Population
Mouse model of myocardial infarction, in vitro bone marrow cells (BMCs), and in ovo models
Design
Preclinical
Key result
Administration of the bifunctional SDF1-GPVI fusion protein in a mouse model of myocardial infarction enhanced recruitment of bone marrow cells, reduced infarct size, and preserved cardiac function.
Authors
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Premature for clinical use; leaves open whether SDF1-GPVI fusion protein aids human post-MI repair.
Does the bispecific SDF1-GPVI fusion protein improve myocardial repair and preserve cardiac function in a mouse model of myocardial infarction?
The novel bispecific SDF1-GPVI fusion protein demonstrates potential for promoting myocardial repair and preserving cardiac function following myocardial infarction in preclinical models.
Ziégler et al. (2012) studied Myocardial infarction. SDF1-GPVI fusion protein was evaluated on Recruitment of BMCs, capillary density, infarct size, and cardiac function. Administration of the bifunctional SDF1-GPVI fusion protein in a mouse model of myocardial infarction enhanced recruitment of bone marrow cells, reduced infarct size, and preserved cardiac function.