Effect of adjuvant Shenqi injection therapy on cardiac function and myocardial fibrosis in patients with refractory heart failure

Objective: To explore the effect of adjuvant Shenqi injection therapy on cardiac function and myocardial fibrosis in patients with refractory heart failure. Methods: Patients with refractory heart failure who were treated in People's Hospital Affiliated to Hubei University of Medicine between December 2014 and August 2016 were reviewed and divided into the control group (n=50) who received routine western medicine treatment and the observation group (n=41) who received Shenqi injection-assisted routine western medicine treatment. The differences in serum levels of cardiac function-related indexes and myocardial fibrosis-related indexes were compared between two groups of patients before and after treatment. Results: Before treatment, the differences in serum levels of cardiac function-related indexes and myocardial fibrosis-related indexes were not statistically significant between the two groups of patients. After 1 month and 3 months of treatment, serum cardiac function-related indexes NT-proBNP, Copeptin, GDF-15 and OPN levels of observation group were lower than those of control group;serum myocardial fibrosis-related indexes TGF-β1, CTGF, PⅠCP, CⅠTP and PⅢNP levels were lower than those of control group whereas APN levels were higher than that of control group. Conclusion: Routine western medicine treatment combined with adjuvant Shenqi injection therapy can effectively optimize the cardiac function and inhibit the myocardial fibrosis process in patients with refractory heart failure.

GTF2H4 regulates partial EndMT via NF-κB activation through NCOA3 phosphorylation in ischemic diseases

Partial endothelial-to-mesenchymal transition(EndMT)is an intermediate phenotype observed in endothelial cells(ECs)undergoing a transition toward a mesenchymal state to support neovascularization during(patho)physiological angiogenesis.Here,we investigated the occurrence of partial EndMT in ECs under hypoxic/ischemic conditions and identified general transcription factor IIH subunit 4(GTF2H4)as a positive regulator of this process.In addition,we discovered that GTF2H4 collaborates with its target protein excision repair cross-complementation group 3(ERCC3)to co-regulate partial EndMT.Furthermore,by using phosphorylation proteomics and site-directed mutagenesis,we demonstrated that GTF2H4 was involved in the phosphorylation of receptor coactivator 3(NCOA3)at serine 1330,which promoted the interaction between NCOA3 and p65,resulting in the transcriptional activation of NF-κB and the NF-kB/Snail signaling axis during partial EndMT.In vivo experiments confirmed that GTF2H4 significantly promoted partial EndMT and angiogenesis after ischemic injury.Collectively,our findings reveal that targeting GTF2H4 is promising for tissue repair and offers potential opportunities for treating hypoxic/ischemic diseases.