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N6-methyladenosine (m6A) methyltransferase METTL3 regulates sepsis-induced myocardial injury through IGF2BP1/HDAC4 dependent manner

This trajectory was marked by features of epithelial-to-mesenchymal transition (EMT), providing a mechanistic explanation for both the shedding of degenerative aTECs into the urine and their contribution to fibroblast accumulation in DKD (Ma et al., 2025b)

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Rest days allow tissue repair and prevent overtraining