Vaginal microbiome is mutually beneficial to the host and has a significant impact on health and disease. Candida species, including Candida albicans, are part of the mucosal flora of most healthy women. Under suitable conditions, they can live in the vulvovaginal mucosa, resulting in symptomatic vulvovaginal candidiasis (VVC). Based on the analysis of 16S ribosomal RNA gene sequences, great progress has been made in exploring the composition and structure of vaginal bacterial community. Moreover, researchers have conducted several studies on whether vaginal microbiome will change during VVC infection. In addition, it has been reported that vaginal colonization of probiotics in vaginal microorganisms, especially Lactobacillus, can effectively reduce the risk of VVC and treat VVC. This review aims to summarize the changes of vaginal microflora during VVC infection, and further point out the possibility of using lactic acid bacteria as probiotics to treat VVC, so as to reduce the adverse consequences of VVC infection and reduce the expensive treatment cost.

In recent years, due to the development and widespread utilization of metagenomic sequencing and metabolomics, the relationship between gut microbiota and human cardiovascular diseases (CVDs) has received extensive attention. A growing number of studies have shown a strong relationship between gut microbiota and CVDs, such as coronary atherosclerosis, hypertension (HTN) and heart failure (HF). It has also been revealed that intestinal flora-related metabolites, such as trimethylamine-N-oxide (TMAO), short-chain fatty acids (SCFA) and bile acids (BAs), are also related to the development, prevention, treatment and prognosis of CVDs. In this review, we presented and summarized the recent findings on the relationship between gut microbiota and CVDs, and concluded several currently known gut microbiota-related metabolites and the occurrence and development of CVDs.

FGF21 is a critical endogenous regulator in energy homeostasis and systemic glucose and lipid metabolism. Despite intensive study of the metabolic functions of FGF21, its important role in heart disease needs further exploration. Apoptosis induced by ox-LDL in vascular endothelial cells is an important step in the progress of atherosclerosis. The effects of FGF21 treatment on apoptosis induced by ox-LDL were tested in HUVECs. The role of FGF21 in atherosclerosis was studied by evaluating its function in apolipoprotein E double knockout (apoE−/−) mice. We found that apoptosis in HUVECs was alleviated by FGF21 treatment. The effects of FGF21 were independent of the ERK1/2 pathway and were mediated through inhibition of the Fas signaling pathway. FGF21 suppressed the development of atherosclerosis, and the administration of FGF21 ameliorated Fas-mediated apoptosis in apoE−/− mice. FGF21 protects against apoptosis in HUVECs by suppressing the expression of Fas; furthermore, FGF21 alleviated atherosclerosis by ameliorating Fas-mediated apoptosis in apoE−/− mice.

Background: It remains unclear whether transfer RNA-derived small RNAs (tsRNAs) play a role in pathological cardiac hypertrophy (PCH). We aimed to clarify the expression profile of tsRNAs and disclose their relationship with the clinical phenotype of PCH and the putative role. Methods: Small RNA sequencing was performed on the plasma of PCH patients and healthy volunteers. In the larger sample size and angiotensin II (Ang II)-stimulated H9c2 cells, the data were validated by real-time qPCR. Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were examined in Ang II-stimulated H9c2 cells. The potential role of tsRNAs in the pathogenesis of PCH was explored by bioinformatics analysis. Results: A total of 4185 differentially expressed tsRNAs were identified, of which four and five tsRNAs were observed to be significantly upregulated and downregulated, respectively. Of the five downregulated tsRNAs, four were verified to be significantly downregulated in the larger sample group, including tRF-30-3JVIJMRPFQ5D, tRF-16-R29P4PE, tRF-21-NB8PLML3E, and tRF-21-SWRYVMMV0, and the AUC values for diagnosis of concentric hypertrophy were 0.7893, 0.7825, 0.8475, and 0.8825, respectively. The four downregulated tsRNAs were negatively correlated with the left ventricular posterior wall dimensions in PCH patients (r = −0.4227; r = −0.4517; r = −0.5567; r = −0.4223). The levels of ANP and BNP, as well as cell size, were decreased in Ang II–stimulated H9c2 cells with 21-NB8PLML3E mimic transfection. Bioinformatics analysis revealed that the target genes of tRF-21-NB8PLML3E were mainly enriched in the metabolic pathway and involved in the regulation of ribosomes. Conclusions: The plasma tRF-21-NB8PLML3E might be considered as a biomarker and offers early screening potential in patients with PCH.

In general, the identification of cholesterol-depleted lipid particles can be inferred from non-high-density lipoprotein cholesterol (non-HDL-C) concentration to apolipoprotein B (apoB) concentration ratio, which serves as a reliable indicator for assessing the risk of cardiovascular disease. However, the ability of non-HDL-C/apoB ratio to predict the risk of long-term mortality among the general population remains uncertain. The aim of this study is to explore the association of non-HDL-C/apoB ratio with long-term all-cause and cardiovascular mortality in adults of the United States. This retrospective cohort study was a further analysis of existing information from the National Health and Nutrition Examination Survey (NHANES). In the ultimate analysis, 12,697 participants from 2005 to 2014 were included. Kaplan-Meier (K-M) curves and the log-rank test were applied to visualize survival differences between groups. Multivariate Cox regression and restricted cubic spline (RCS) models were applied to evaluate the association of non-HDL-C/apoB ratio with all-cause and cardiovascular mortality. Subgroup analysis was conducted for the variables of age, sex, presence of coronary artery disease, diabetes and hypertriglyceridemia and usage of lipid-lowering drugs. The average age of the cohort was 46.8 ± 18.6 years, with 6215 (48.9%) participants being male. During a median follow-up lasting 68.0 months, 891 (7.0%) deaths were documented and 156 (1.2%) patients died of cardiovascular disease. Individuals who experienced all-cause and cardiovascular deaths had a lower non-HDL-C/apoB ratio compared with those without events (1.45 ± 0.16 vs. 1.50 ± 0.17 and 1.43 ± 0.17 vs. 1.50 ± 0.17, both P values < 0.001). The results of adjusted Cox regression models revealed that non-HDL-C/apoB ratio exhibited independent significance as a risk factor for both long-term all-cause mortality [hazard ratio (HR) = 0.51, 95% confidence interval (CI): 0.33–0.80] and cardiovascular mortality (HR = 0.33, 95% CI: 0.12–0.90). Additionally, a significant sex interaction was discovered (P for interaction <0.05), indicating a robust association between non-HDL-C/apoB ratio and long-term mortality among females. The RCS curve showed that non-HDL-C/apoB ratio had a negative linear association with long-term all-cause and cardiovascular mortality (P for non-linearity was 0.098 and 0.314). The non-HDL-C/apoB ratio may serve as a potential biomarker for predicting long-term mortality among the general population, independent of traditional risk factors.