Current therapies for cardiac ischemia-reperfusion (I/R) injury remain insufficient.This study identifies PDE4D as a novel promotor of myocardial I/R injury, addressing the unmet need for new therapeutic targets.We further reveal that METTL14-mediated N6methyladenosine modification stabilizes PDE4D mRNA via the reader IGF2BP1, a previously unknown regulatory axis.Scientifically, this uncovers a new epitranscriptomic mechanism controlling cardiomyocyte apoptosis.Clinically, targeting the METTL14/IGF2BP1/PDE4D axis could offer a promising strategy for mitigating cardiac I/R injury.
Li et al. (Thu,) studied this question.