Key result
Myeloid cell-specific Smad7 loss in a mouse model of myocardial infarction did not affect cardiac dysfunction, chamber dilation, scar remodeling, collagen deposition, or macrophage recruitment.
Why the study?
Macrophage Smad7 was hypothesized to regulate post-myocardial infarction inflammation and fibrosis by suppressing TGF-beta responses or through TGF-independent actions.
Population
Mouse model of myocardial infarction and in vitro macrophages
Comparison
Myeloid cell-specific Smad7 loss vs intact Smad7
Design
Preclinical animal and in vitro laboratory study
Authors
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Macrophage Smad7 may modulate post-MI inflammation and fibrosis in mice; leaves open translational relevance to human remodeling.
Endogenous Smad7 in macrophages plays a limited role in regulating post-infarction inflammation and repair, and does not restrain the anti-inflammatory effects of TGF-β.
Li et al. (2022) studied Myocardial infarction. Myeloid cell-specific Smad7 loss vs. Control was evaluated on Cardiac dysfunction, chamber dilation, scar remodeling, collagen deposition, and macrophage recruitment. Myeloid cell-specific Smad7 loss in a mouse model of myocardial infarction did not affect cardiac dysfunction, chamber dilation, scar remodeling, collagen deposition, or macrophage recruitment.
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