No abstract

No abstract

No abstract

Background. Atherosclerosis (AS) is a common chronic vascular inflammatory disease and one of the main causes of cardiovascular/cerebrovascular diseases (CVDs). Autophagy-related genes (ARGs) play a crucial part in pathophysiological processes of AS. However, the expression profile of ARGs has rarely been adopted to explore the relationship between autophagy and AS. Therefore, using the expression profile of ARGs to explore the relationship between autophagy and AS may provide new insights for the treatment of CVDs. Methods. The differentially expressed ARGs of the GSE57691 dataset were obtained from the Human Autophagy Database (HADb) and the Gene Expression Omnibus (GEO) database, and the GSE57691 dataset contains 9 aortic atheroma tissues and 10 normal aortic tissues. The differentially expressed ARGs of the GSE57691 dataset were analyzed by protein-protein interaction (PPI), gene ontology analysis (GO), and Kyoto Encyclopedia of Genes and Genomes analysis (KEGG) and were chosen to explore related miRNAs/transcriptional factors. Results. The GSE57691 dataset had a total of 41 differentially expressed ARGs. The GO analysis results revealed that ARGs were mainly enriched in autophagy, autophagosome, and protein serine/threonine kinase activity. KEGG analysis results showed that ARGs were mainly enriched in autophagy-animal and longevity regulating signaling pathways. Expressions of ATG5, MAP1LC3B, MAPK3, MAPK8, and RB1CC1 were regarded as focus in the PPI regulatory networks. Furthermore, 11 related miRNAs and 6 related transcription factors were obtained by miRNAs/transcription factor target network analysis. Conclusions. Autophagy and ARGs may play a vital role in regulating the pathophysiology of AS.

Vascular smooth muscle cells (VSMCs) excessive migration, a basic change of pathological intimal thickening, can lead to serious cardiovascular diseases such as atherosclerosis, myocardial infarction, and stroke. Ligustilide (LIG), the main active ingredient of angelica volatile oil, has been demonstrated to exert protective effects on the cardiovascular and cerebrovascular, circulatory system, and immune function. However, whether it protects against intimal thickening and VSMCs excessive migration and its underlying mechanism remains largely unknown. The aim of this study is to investigate the effect of LIG on VSMCs migration and its underlying mechanism. The protective effect of LIG on VSMCs excessive migration was assessed using an atherosclerotic spontaneously hypertensive rat model and an angiotensin II (AngII)-induced VSMCs migration model. The results showed that LIG exerted a protective effect against pathological intimal thickening as demonstrated by decreasing VSMCs migration in vivo and in vitro. In vivo, intimal thickening and VSMCs migration were inhibited and LIG performed a suppressive effect on the expression of c-Myc protein while enhanced phenotypic transformation related proteins α-SMA expression. Meanwhile, the administration of LIG significantly lowered the blood pressure and blood lipids level in atherosclerotic spontaneously hypertensive rats. In vitro, LIG suppressed AngII-induced VSMCs migration and downregulated the expression of migration related protein c-Myc, MMP2, ROCK1, ROCK2, p-JNK, and JNK. These findings suggested the protective effect of LIG on VSMCs migration was associated with the decrement of c-Myc/MMP2 signaling pathway and ROCK-JNK signaling pathway. Thus, LIG may serve as a novel therapeutic agent for preventing cardiovascular disease.