miR-21 promotes cardiac fibrosis after myocardial infarction by targeting Smad7, highlighting it as a potential therapeutic target.
miR-21 inhibition may reduce post-MI fibrosis; hypothesis-generating in animal models only.
These findings suggested that miR-21 has a critical role in CF activation and cardiac fibrosis after MI through via TGF-β/Smad7 signaling pathway. Thus, miR-21 promises to be a potential therapy in treatment of cardiac fibrosis after MI.
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Yuan et al. (2017) studied this question.
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