Tenascin-C accelerates adverse left ventricular remodeling after myocardial infarction by modulating macrophage polarization.
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TN-C-macrophage effects in experimental MI are hypothesis-generating; leaves open translation to human remodeling therapies.
These results suggested that TN-C accelerates LV remodelling after MI, at least in part, by modulating M1/M2-macrophage polarization.
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Kimura et al. (2018) studied this question.
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