Key result
Bone marrow transplantation of wild-type HSPCs in c-kit-deficient mice rescued cardiac repair after myocardial infarction by mediating natural killer and angiogenic cell mobilization.
Why the study?
Does bone marrow transplantation of wild-type HSPCs improve cardiac repair and function in c-kit-deficient mice after myocardial infarction?
Does bone marrow transplantation of wild-type HSPCs improve cardiac repair and function in c-kit-deficient mice after myocardial infarction?
c-kit signaling plays a crucial role in cardiac repair after myocardial infarction by mediating bone marrow-derived natural killer and angiogenic cell mobilization.
No takes yet. Share an insight, caveat, or question.
Should not alter post-MI care; hypothesis-generating for c-kit/HSPC-mediated repair in mice.
Ayach et al. (2006) studied Myocardial infarction. Bone marrow transplantation of wild-type HSPCs vs. c-kit-deficient mice without transplantation was evaluated on Cardiac repair, ventricular dilation, hypertrophy, and cardiac function. Bone marrow transplantation of wild-type HSPCs in c-kit-deficient mice rescued cardiac repair after myocardial infarction by mediating natural killer and angiogenic cell mobilization.
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