Taken together, lncRNA MALAT1 interacting with EZH2 stimulated AKT-1 phosphorylation and decreased BRCA1 expression, consequently aggravating the progression of sepsis, highlighting a promising therapeutic option for sepsis.
These results suggest that the MALAT1/hsa-miR-346/SMAD3 regulatory network plays a key role in the development of sepsis, and may serve as a target for the treatment of sepsis.
MALAT1 knockdown significantly increased LVSP and +dp/dsmax, decreased LVEDP and -dp/dsmax of sepsis as well as levels of cTn-I, CK, CK-MB, TNF-α, IL-1β, IL-6, IL-10, IL-17, IFN-γ, C5 and C5a.