Key result
Deletion of epicardial YAP/TAZ in mice exacerbated post-myocardial infarction fibrosis (65.4% vs 43.4% in controls) and inflammation due to impaired recruitment of suppressive regulatory T cells.
Why the study?
Does epicardial YAP/TAZ deletion exacerbate post-MI fibrosis and inflammation, and can local IFN-γ delivery rescue this phenotype in mice?
Does epicardial YAP/TAZ deletion exacerbate post-MI fibrosis and inflammation, and can local IFN-γ delivery rescue this phenotype in mice?
Absolute Event Rate: 65.4% vs 43.4%
p-value: p=<0.05
Epicardial Hippo signaling (YAP/TAZ) is crucial for suppressing post-MI inflammation and fibrosis by recruiting Tregs via IFN-γ, suggesting a potential therapeutic target for post-MI remodeling.
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Epicardial YAP/TAZ deletion worsens post-MI fibrosis in mice; hypothesis-generating for Hippo modulation in human remodeling.
Ramjee et al. (2017) studied Myocardial Infarction. Epicardial YAP/TAZ deletion vs. Control (Yapfl/fl Tazfl/fl mice) was evaluated on Fibrotic scarring as a percentage of the left ventricular free wall cross-sectional area 14 days after MI (p=<0.05). Deletion of epicardial YAP/TAZ in mice exacerbated post-myocardial infarction fibrosis (65.4% vs 43.4% in controls) and inflammation due to impaired recruitment of suppressive regulatory T cells.
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