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Consequently, this research was intended to investigate the effects of tripartite motif protein 11 on cardiomyocytes I/R injury and the underlying mechanism. Following the detection of oxidative stress-related pathways by TRIM11 downregulation in I/R cells, cell proliferation, and apoptosis at 48 h, as well as the associated molecular changes in oxidative stress-related pathways, oxidative stress responses were reported. In addition, the overexpression of TRIM11 in AC16 cells led to apoptosis in AC16 cells, and JNK1/2 inhibition and DUSP1 overexpression potently countered the initiation of TRIM11 overexpression in AC16 cells. The downregulation of TRIM11 reduces apoptosis in AC16 cells after I/R injuries, most likely through the DUSP1-JNK1/2 pathways, according to these.
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