Key result
Macrophage NCOR1 deficiency significantly reduced infarct size, improved cardiac function after MI, and inhibited neointimal hyperplasia in a mouse model.
Why the study?
The function of macrophage NCOR1 in response to myocardial infarction or vascular wire injury had not been elucidated.
Does macrophage NCOR1 deficiency improve outcomes in mouse models of myocardial infarction and arterial wire injury?
Population
Macrophage Ncor1 knockout mice and cultured primary macrophages
Comparison
Macrophage Ncor1 knockout vs control
Design
Animal and cell culture experimental study
Authors
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Supports macrophage NCOR1 as a potential post-MI target; leaves open translation to human therapy.
Does macrophage NCOR1 deficiency improve outcomes in mouse models of myocardial infarction and arterial wire injury?
Macrophage NCOR1 deficiency attenuates myocardial infarction and neointimal hyperplasia in mice by reducing inflammation and macrophage proliferation, suggesting it as a potential therapeutic target.
Du et al. (2020) studied Myocardial infarction and neointimal hyperplasia. Macrophage NCOR1 deficiency (Ncor1 knockout) vs. Control mice/cells was evaluated on Infarct size, cardiac function, and neointimal hyperplasia. Macrophage NCOR1 deficiency significantly reduced infarct size, improved cardiac function after MI, and inhibited neointimal hyperplasia in a mouse model.
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