Gut microbiota ( GM ) is a collection of bacteria, fungi, archaea, viruses and protozoa , etc. They inhabit human intestines and play an essential role in human health and disease. Close information exchange between the intestinal microbes and the host performs a vital role in digestion, immune defence, nervous system regulation, especially metabolism, maintaining a delicate balance between itself and the human host. Studies have shown that the composition of GM and its metabolites are firmly related to the occurrence of various diseases. More and more researchers have demonstrated that the intestinal microbiota is a virtual ‘organ’ with endocrine function and the bioactive metabolites produced by it can affect the physiological role of the host. With deepening researches in recent years, clinical data indicated that the GM has a significant effect on the occurrence and development of cardiovascular diseases ( CVD ). This article systematically elaborated the relationship between metabolites of GM and its effects, the relationship between intestinal dysbacteriosis and cardiovascular risk factors, coronary heart disease, myocardial infarction, heart failure and hypertension and the possible pathogenic mechanisms. Regulating the GM is supposed to be a potential new therapeutic target for CVD .

Myocardial fibrosis (MF) is the result of metabolic imbalance of collagen synthesis and metabolism, which is widespread in various cardiovascular diseases. Autophagy is a lysosomal degradation pathway which is highly conserved. In recent years, research on autophagy has been increasing and the researchers have also become cumulatively aware of the specified association between autophagy and MF. This review highlights the role of autophagy in MF and the potential effects through the administration of medicine.

Background: It has been reported that atractylodin has a potential antitumor effect. This study aimed to investigate the effects of atractylodin on Huh7 and Hccm hepatocellular carcinoma (HCC) cells and its molecular mechanism.Methods: Huh7 and Hccm cells were cultured in vitro, and their viability was detected by CCK-8 assay and the half inhibitory concentration (IC50) was calculated. The cells were treated with different concentrations of atractylodin, and the migration and invasion ability of cells was detected by scratch assay and Transwell assay. The cell cycle change and apoptosis rate were detected by flow cytometry. IlluminaHiSeq4000 platform was used for transcriptome sequencing, and the results were analyzed for gene differential expression, gene function, and signal pathway enrichment. Morphological changes of cells were detected by transmission electron microscopy, reactive oxygen species (ROS) levels were detected by DCFH-DA probe, and the expressions of ferroptosis related proteins GPX4, ACSL4, FTL, and TFR1 were detected by Western blot. Results:The results showed that atractylodin could inhibit the proliferation, migration, and invasion of Huh7 and Hccm cells, regulate the cell cycle, and induce cell apoptosis and G1 phase cell cycle arrest. In addition, it could significantly induce the increase of intracellular ROS levels, decrease the expression of GPX4 and FTL proteins, and up-regulate the expression of ACSL4 and TFR1 proteins.Conclusions: Atractylodin can inhibit the proliferation, migration, and invasion of Huh7 and Hccm liver cancer cells, and induce cell apoptosis and cell cycle arrest. In addition, our results suggest that atractylodin may induce ferroptosis in HCC cells by inhibiting the expression of GPX4 and FTL proteins, and upregulating the expression of ACSL4 and TFR1 proteins.

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Myocardial fibrosis is characterized by the metabolic imbalance of collagen synthesis and metabolism, which leads to pathological change of myocardial remodelling, and mostly seen in various cardiovascular diseases. 1 Myocardial fibrosis is categorized into reactive fibrosis and reparative fibrosis. 2 Reactive fibrosis occurs in the myocardial hypertrophy caused by excessive heart pressure without myocardial cell loss, whereas reparative fibrosis occurs in acute myocardial ischaemia and dilated cardiomyopathy. Both can affect the myocardial collagen content and promote myocardial diastolic and/or contractile dysfunction. Reparative myocardial fibrosis is the pathological basis for the development of myocarditis and post-inflammatory dilated cardiomyopathy to refractory heart failure, promoting the deterioration of the diseased heart function in dilated myocardium. 3 Therefore, reversing myocardial remodelling might add value to the treatment of dilated cardiomyopathy. 4 Dilated cardiomyopathy is complex heterogeneous cardiomyopathy characterized by ventricular enlargement and reduced myocardial contractile function, with a 5-year mortality rate of 15%-50%. 5 Among all the factors such as infection, autoimmunity, cellular immunity and genetics, autoimmune reactions