Metabolic syndrome (MetS) and short sleep are prevalent health concerns in the United States, yet the relationship between leisure-time physical activity (LTPA) and MetS among individuals with short sleep duration remains unclear. This cross-sectional study analyzed data from 8999 US adults aged 20 years and older in the National Health and Nutrition Examination Survey. Short sleep duration was defined as less than 7 h per night, and MetS was diagnosed based on criteria from the American Endocrine Society and the American Society of Clinical Endocrinology. Weighted regression analyses revealed a significant inverse association between LTPA and MetS, with higher LTPA levels linked to lower MetS (OR (95% CI): 0.990 (0.984, 0.997), p = 0.003). Participants who achieved the World Health Organization’s recommended LTPA levels had a substantially lower MetS compared to those with no LTPA (OR (95% CI): 0.624 (0.527, 0.738), p = 0.001). Stratified analyses showed that this protective effect varied across demographic subgroups, and a threshold effect was observed at 2000 MET-min/week, beyond which further LTPA did not significantly enhance protection against MetS. These findings highlight the importance of regular LTPA that is negatively associated with MetS among individuals with inadequate sleep, emphasizing the need for targeted health promotion efforts in this population.

Background: Myocardial infarction (MI) represents a severe cardiovascular disease with limited therapeutic agents. This study was aimed to elucidate the role of the exosomes derived from human placental mesenchymal stem cells (PMSCs-Exos) in MI. Methods: PMSCs were isolated and cultured in vitro, with identification by both transmission electron microscopy (TEM) and nanoparticle tracking analysis (NTA). To further investigate the effects of PMSC-Exos on MI, C57BL/6 mice were randomly divided into Sham group, MI group, and PMSC-Exos group. After 4 weeks of the intervention, cardiac function was assessed by cardiac echocardiography, electrocardiogram and masson trichrome staining; lipid indicators were determined by automatic biochemical instrument; inflammatory cytokines were measured by cytometric bead array (CBA); gut microbiota, microbial metabolites short chain fatty acids (SCFAs) as well as lipopolysaccharide (LPS) were separately investigated by 16S rRNA high throughput sequencing, gas chromatography mass spectrometry (GC–MS) and tachypleus amebocyte lysate kit; transcriptome analysis was used to test the transcriptional components (mRNA\miRNA\cirRNA\lncRNA) of PMSC-Exos. Results: We found that human PMSC-Exos were obtained and identified with high purity and uniformity. MI model was successfully established. Compared to MI group, PMSC-Exos treatment ameliorated myocardial fibrosis and left ventricular (LV) remodeling (P < 0.05). Moreover, PMSC-Exos treatment obviously decreased MI molecular markers (AST/BNP/MYO/Tn-I/TC), pro-inflammatory indicators (IL-1β, IL-6, TNF-α, MCP-1), as well as increased HDL in comparison with MI group (all P < 0.05). Intriguingly, PMSC-Exos intervention notably modulated gut microbial community via increasing the relative abundances of Bacteroidetes, Proteobacteria, Verrucomicrobia, Actinobacteria, Akkermansia, Bacteroides, Bifidobacterium, Thauera and Ruminiclostridium, as well as decreasing Firmicutes (all P < 0.05), compared with MI group. Furthermore, PMSC-Exos supplementation increased gut microbiota metabolites SCFAs (butyric acid, isobutyric acid and valeric acid) and decreased LPS in comparison with MI group (all P < 0.05). Correlation analysis indicated close correlations among gut microbiota, microbial SCFAs and inflammation in MI. Conclusions: Our study highlighted that PMSC-Exos intervention alleviated MI via modulating gut microbiota and suppressing inflammation.

Atherosclerosis (AS) is closely associated with chronic low-grade inflammation and gut dysbiosis. Metformin (MET) presents pleiotropic benefits in the control of chronic metabolic diseases, but the impacts of MET intervention on gut microbiota and inflammation in AS remain largely unclear. In this study, ApoE^-/- mice with a high-fat diet (HFD) were adopted to assess the MET treatment. After 12 weeks of MET intervention (100mg·kg^-1·d^-1), relevant indications were investigated. As indicated by the pathological measurements, the atherosclerotic lesion was alleviated with MET intervention. Moreover, parameters in AS including body weights (BWs), low-density lipoprotein (LDL), triglyceride (TG), total cholesterol (TC) and malondialdehyde (MDA) were elevated; whereas high-density lipoprotein (HDL) and total superoxide dismutase (T-SOD) levels were decreased, which could be reversed by MET intervention. Elevated pro-inflammatory interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α and lipopolysaccaride (LPS) in AS were decreased after MET administration. However, anti-inflammatory IL-10 showed no significant difference between AS group and AS+MET group. Consistently, accumulated macrophages in the aorta of AS were conversely lowered with MET treatment. The results of 16S rRNA sequencing and analysis displayed that the overall community of gut microbiota in AS was notably changed with MET treatment mainly through decreasing Firmicutes, Proteobacteria, Romboutsia, Firmicutes/Bacteroidetes, as well as increasing Akkermansia, Bacteroidetes, Bifidobacterium. Additionally, we found that microbiota-derived short-chain fatty acids (SCFAs) including acetic acid, propionic acid, butyric acid and valeric acid in AS were decreased, which were significantly up-regulated with MET intervention. Consistent with the attenuation of MET on gut dysbiosis, decreased intestinal tight junction protein zonula occludens-1 (ZO)-1 in AS was restored after MET supplementation. Correlation analysis showed close relationships among gut bacteria, microbial metabolites SCFAs and inflammation. Collectively, MET intervention ameliorates AS in ApoE^-/- mice through restoring gut dysbiosis and anti-inflammation, thus can potentially serve as an inexpensive and effective intervention for the control of the atherosclerotic cardiovascular disease.

The study investigated the cardiovascular effects of daily exposure to plastic products by simulating the oral heat exposure mode of disposable plastic takeout containers (DPTC) commonly used in society. Questionnaires were used to randomly choose 3179 people in order to examine any possible correlation between the frequency of plastic exposure and the risk of cardiovascular diseases (CVD). Additionally, Sprague-Dawley(SD) rats consumed leachate from DPTC exposed to boiling water for 1 minute，5 minutes and 15 minutes respectively, over three months. After intervention, fecal samples were taken for microbiota and metabolomics analysis, and rat cardiac tissue was studied by staining and electron microscopy. Serum parameters were tested to analyze cardiovascular system changes. The population-based plastic exposure questionnaire data revealed that high-frequency exposure to plastics is significantly associated with an increased risk of congestive heart failure, with an odds ratio of 1.13 (95 % CI: 1.03-1.24). Rat fecal analysis revealed that β diversity and composition of gut microbiota in experimental groups were changed. Inflammatory cell infiltration, mitochondrial swelling, and serum indicators of oxidative stress and inflammation were significantly elevated in the myocardium, without temporal differences observed. The study shows plastic exposure as a significant CVD risk factor regardless of duration. It leads to changes in myocardial tissue, gut microbiota, and metabolites, all closely tied to CVD.

Background: Abdominal aortic calcification (AAC) is one of the earliest observed forms of atherosclerotic calcification and is crucial for early cardiovascular risk prediction. Frailty, a global clinical and public health challenge, is associated with increased risks of mortality, functional decline, and loss of independence. However, the relationship between the Frailty Index (FI) and AAC among middle-aged and older adults has yet to be explored.Methods: This study analyzed data from 2013 to 2014 National Health and Nutrition Examination Survey (NHANES) cohort, focusing on individuals aged ≥ 40 years. The FI was calculated using a 49-item model to assess frailty status and participants were stratified into three groups: non-frail (FI ≤ 0.15), pre-frail (0.15 < FI ≤ 0.25), and frail (FI > 0.25). AAC was measured by dual-energy X-ray absorptiometry and quantified by Kauppila scores. Severe AAC was defined as an AAC score > 6. The relationship between FI and AAC was investigated using multivariable logistic regression, sensitivity analyses, and smoothing curve fitting. Subgroup analyses and interaction tests were conducted to assess the stability of this association across different populations.Results: A total of 2,572 participants were enrolled in this study. Following adjustment for potential confounders, FI exhibited a statistically significant positive association with both AAC score (β = 2.64, 95%CI = 1.20–4.08) and Severe AAC (OR = 6.36, 95%CI = 1.48–27.41). Similar trends (P for trend < 0.05) were observed when FI was analyzed as a categorical variable. Smooth curve fitting and subgroup analysis were used to investigate the relationship between baseline FI Z-score and AAC score and Severe AAC. Interestingly, we found that the FI Z-score was linearly related to the occurrence of severe AAC, while it was nonlinearly related to the AAC score. The FI-Z score was positively associated with the likelihood of AAC score before the breakpoint (K = 0.78), but not significant after the breakpoint. The association between FI-Z score and Severe AAC was stable in the different subgroups (all P for interaction > 0.05).Conclusion: Our study indicated a stable positive correlation between FI and AAC. FI may serve as a biomarker for early subclinical atherosclerosis detection in middle-aged and older US adults.