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doi: 10.1080/07853890802322229 63 KennedyEPLehningerAL

Mechanistically, DUSP4-mediated phosphorylation of YTHDC1 at threonine residue T148 enhances its binding to SRSF3, thereby reducing nuclear retention of FTH1/FTL mRNA

These results suggest that inhibition of HDAC can maintain cardiac function and attenuate cardiac remodeling by stimulating endogenous cardiac regeneration