Sepsis is a life-threatening condition caused by a dysregulated host response to infection,with its high mortality closely linked to excessive neutrophil activation and the release of neutrophil extracellular traps(NE...Sepsis is a life-threatening condition caused by a dysregulated host response to infection,with its high mortality closely linked to excessive neutrophil activation and the release of neutrophil extracellular traps(NETs).While NETs play a critical role in antimicrobial immunity,their overproduction can lead to tissue damage and multiple organ dysfunction,exacerbating the pathological progression of sepsis.This study focuses on the role of palmitoyltransferase ZDHHC18 in sepsis,proposing that it may regulate the formation of neutrophil NETs through palmitoylation,thereby promoting the onset of sepsis.Currently,there is no research,domestically or internationally,on the role of ZDHHC18 in NETs during sepsis.Therefore,exploring potential therapeutic strategies—such as inhibiting ZDHHC18 to mitigate the pathological effects of sepsis—could provide new insights for treating sepsis-related inflammatory diseases.展开更多
Exosomes have shown good potential in ischemic injury disease treatments.However,evidence about their effect and molecular mechanisms in osteonecrosis of femoral head(ONFH)treatment is still limited.Here,we revealed t...Exosomes have shown good potential in ischemic injury disease treatments.However,evidence about their effect and molecular mechanisms in osteonecrosis of femoral head(ONFH)treatment is still limited.Here,we revealed the cell biology characters of ONFH osteonecrosis area bone tissue in single cell scale and thus identified a novel ONFH treatment approach based on M2 macrophages-derived exosomes(M2-Exos).We further show that M2-Exos are highly effective in the treatment of ONFH by modulating the phenotypes communication between neutrophil and endothelium including neutrophil extracellular traps formation and endothelial phenotype transition.Additionally,we identified that M2-Exos’therapeutic effect is attributed to the high content of miR-93-5p and constructed miR-93-5p overexpression model in vitro and in vivo based on lentivirus and adenoassociated virus respectively.Then we found miR-93-5p can not only reduce neutrophil extracellular traps formation but also improve angiogenic ability of endothelial cells.These results provided a new theoretical basis for the clinical application of ONFH therapeutic exosomes.展开更多
文摘Sepsis is a life-threatening condition caused by a dysregulated host response to infection,with its high mortality closely linked to excessive neutrophil activation and the release of neutrophil extracellular traps(NETs).While NETs play a critical role in antimicrobial immunity,their overproduction can lead to tissue damage and multiple organ dysfunction,exacerbating the pathological progression of sepsis.This study focuses on the role of palmitoyltransferase ZDHHC18 in sepsis,proposing that it may regulate the formation of neutrophil NETs through palmitoylation,thereby promoting the onset of sepsis.Currently,there is no research,domestically or internationally,on the role of ZDHHC18 in NETs during sepsis.Therefore,exploring potential therapeutic strategies—such as inhibiting ZDHHC18 to mitigate the pathological effects of sepsis—could provide new insights for treating sepsis-related inflammatory diseases.
基金the support of the National Natural Science Foundation of China (Grant No.82272503)Natural Science Foundation of Zhejiang Province (Grant No. LQN25H060006)
文摘Exosomes have shown good potential in ischemic injury disease treatments.However,evidence about their effect and molecular mechanisms in osteonecrosis of femoral head(ONFH)treatment is still limited.Here,we revealed the cell biology characters of ONFH osteonecrosis area bone tissue in single cell scale and thus identified a novel ONFH treatment approach based on M2 macrophages-derived exosomes(M2-Exos).We further show that M2-Exos are highly effective in the treatment of ONFH by modulating the phenotypes communication between neutrophil and endothelium including neutrophil extracellular traps formation and endothelial phenotype transition.Additionally,we identified that M2-Exos’therapeutic effect is attributed to the high content of miR-93-5p and constructed miR-93-5p overexpression model in vitro and in vivo based on lentivirus and adenoassociated virus respectively.Then we found miR-93-5p can not only reduce neutrophil extracellular traps formation but also improve angiogenic ability of endothelial cells.These results provided a new theoretical basis for the clinical application of ONFH therapeutic exosomes.
