Mechanistically, α-KG promoted the binding of ten-eleven translocase enzyme (TET1) to the upstream elements of TGFBR2 and TGFBR3 genes, respectively, which reduced methylation and hydroxymethylation enrichment in the intron region of the pro-fibrosis genes TGFBR2 and TGFBR3 to downregulate their transcriptional expression, thereby reversing cardiac fibrosis in rats with DCM. This evidence concerns the gene TGFBR2 and familial dilated cardiomyopathy.