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. 2021 Feb 27;20:55. doi: 10.1186/s12933-021-01245-2

Fig. 1.

Fig. 1

The possible therapeutic mechanism of miRNAs-contributed to the oxidative stress, inflammation and cardiomyocytes function process in diabetic cardiomyopathy. Bcl-2 B-cell lymphoma 2, CASP Caspase, Col4α1 collagen type IV alpha 1, CPDT 5,6 Dihydrocyclopenta-1,2-dithiole-3-thione, DCM diabetic cardiomyopathy, ELAVL1 ELAV like protein 1, FGF1 fibroblast growth factor 1, ERK1/2 extracellular signal-regulated kinases 1 and 2, FOXO3a Forkhead box O3, HOTAIR HOX transcript antisense intergenic RNA, IL interleukin, IRAK1 interleukin-1 receptor-associated kinase 1, LAZ3 lymphoma-associated zinc finger 3, LncRNA long non-coding RNA, MDA malondialdehyde, MiR MicroRNA, MMP-9 matrix metalloproteinase 9, NF-κB nuclear factor kappa-light-chain-enhancer of activated B cells, Nrf2: nuclear factor erythroid 2-related factor 2, PI3K/Akt phosphoinositide 3-kinase and protein kinase B, PPARα peroxisome proliferator-activated receptor-alpha, ROS reactive oxygen species, SIRT-1 Sirtuin 1, SMAD7 SMAD family member 7, SOD superoxide dismutase, TGF-β1 transforming growth factor β1, TNFα tumor necrosis factor-alpha, TRAF6 TNF receptor associated factor 6