Why the study?
MLK3 is associated with CHF and cardiomyocyte injury protection, but its function in myocardial fibrosis remains unknown.
Does inhibition of MLK3 improve cardiac function and remodeling in TAC mice?
Does inhibition of MLK3 improve cardiac function and remodeling in TAC mice?
MLK3 signaling induces pyroptosis and ferroptosis leading to myocardial fibrosis in pressure overload, and its inhibition via miR-351 improves cardiac function.
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Supports MLK3 inhibition in experimental pressure overload; leaves open translation to human HF.
Wang et al. (2020) studied this question.
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