AI Article Synopsis
- FAM46C is linked to sepsis-induced myocardial dysfunction (SIMD), which is critical in predicting sepsis outcomes.
- The study found that FAM46C can reduce cell apoptosis caused by lipopolysaccharides (LPS) in cardiac cells, with its effect mediated through specific signaling pathways.
- This research highlights the potential of FAM46C as a therapeutic target to mitigate myocardial dysfunction in sepsis, marking the first exploration of its role in SIMD.
Article Abstract
Aims: Sepsis is a syndrome of inflammatory response induced by infection. Cellular adhesion molecules may involve in sepsis-induced myocardial dysfunction (SIMD) which is a major predictor of morbidity and mortality of sepsis. Here we studied the role of FAM46C in AC16 cells and c57 mice with lipopolysaccharides (LPS) treatment.
Main Methods: Real-time PCR and western blot were used to detect the expression level of relative genes and protein. Cell proliferation and apoptosis were evaluated.
Key Findings: Interestingly, negative correlation between Toll-like receptor 4 (TLR4) and FAM46C in sepsis was observed. The overexpression of FAM46C reduced the apoptosis induced by LPS in AC16 cells. Inhibition of apoptosis contributed by FAM46C was mediated by adhesion molecule via blocking p38 and ERK/MAPK signaling pathway. Moreover, overexpression of Fam46c and inhibition of TLR4 by TAK-242 could attenuate apoptosis induced by LPS in vivo.
Significance: FAM46C played an important role in SIMD via inhibiting LPS-induced myocardial dysfunction by downregulating cellular adhesion molecules and inhibiting apoptosis. It was the first time to explore the role of FAM46C in SIMD in this study.
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| http://dx.doi.org/10.1016/j.lfs.2019.03.048 | DOI Listing |
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