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In vitro, the aim of this study was to investigate the potential role of FAM129B in regulating hypoxia/reoxygenation-induced cardiomyocyte injury. FAM129B was reduced in cardiomyocyte expression by H/R in accordance with our study. Functional experiments showed that the upregulation of FAM129B improved H/R-exposed cardiomyocyte viability, as well as reduced H/R-induced cardiomyocyte apoptosis, the production of reactive oxygen species and pro-inflammatory cytokine release. The upregulation of FAM129B has significantly raised the nuclear expression of nuclear factor-erythroid 2-related factor 2 in nuclear cells, as well as enhanced Nrf2/antioxidant response element activation in H/R-exposed cardiomyocytes.
Source link: https://europepmc.org/article/MED/34995000
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