Objective    To analyze the factors influencing the occurrence of subclinical leaflet thrombosis (SLT) after percutaneous aortic valve replacement using balloon-expandable valve (Sapien3, S3). Methods     Retrospective analysis was made on 62 patients with severe aortic stenosis undergoing percutaneous aortic valve replacement using S3 in our center from September 2020 to June 2022. Patients with a history of vascular atherosclerosis or with significant increase or insignificant decrease of aortic valve flow or gradient pressure during follow-up were selected for CT examination. Results     A total of 26 patients were finally included, with an average age of 70.31±8.90 years, and the male proportion was higher (n=15, 57.69%). Among them, 5 patients had SLT. Compared with the non-SLT group, patients in the SLT group were older (68.52±8.80 years vs. 77.80±4.66 years, P=0.007). The age factor (≥75 years) and the diameter of the ascending aorta were associated with SLT (both P<0.05). Conclusion     The incidence of SLT is higher in the elderly patients. It is speculated that SLT is related to the characteristics of short balloon dilation valves and low blood flow dynamics of valve racks.

Mitochondria as a signaling platform play crucial roles in deciding cell fate. Many classic anticancer agents are known to trigger cell death through induction of mitochondrial damage. Mitophagy, one selective autophagy, is the key mitochondrial quality control that effectively removes damaged mitochondria. However, the precise roles of mitophagy in tumorigenesis and anticancer agent treatment remain largely unclear. Here, we examined the functional implication of mitophagy in the anticancer properties of magnolol, a natural product isolated from herbal

Metastasis is crucial for the mortality of non-small cell lung carcinoma (NSCLC) patients. The epithelial-mesenchymal transition (EMT) plays a critical role in regulating tumor metastasis. Glioma-associated oncogene 1 (Gli1) is aberrantly active in a series of tumor tissues. However, the molecular regulatory relationships between Gli1 and NSCLC metastasis have not yet been identified. Herein, we reported Gli1 promoted NSCLC metastasis. High Gli1 expression was associated with poor survival of NSCLC patients. Ectopic expression of Gli1 in low metastatic A549 and NCI-H460 cells enhanced their migration, invasion abilities and facilitated EMT process, whereas knock-down of Gli1 in high metastatic NCI-H1299 and NCI-H1703 cells showed an opposite effect. Notably, Gli1 overexpression accelerated the lung and liver metastasis of NSCLC in the intravenously injected metastasis model. Further research showed that Gli1 positively regulated Snail expression by binding to its promoter and enhancing its protein stability, thereby facilitating the migration, invasion and EMT of NSCLC. In addition, administration of GANT-61, a Gli1 inhibitor, obviously suppressed the metastasis of NSCLC. Collectively, our study reveals that Gli1 is a critical regulator for NSCLC metastasis and suggests that targeting Gli1 is a prospective therapy strategy for metastatic NSCLC.