Association of changes in lipids with risk of myocardial infarction among people without lipid-lowering therapy

Tian, Xue; Zuo, Yingting; Chen, Shuohua; Li, Haibin; He, Yan; Zhang, Licheng; An, Jee Hyun; Wu, Shouling; Luo, Yanxia; Wang, Anxin

doi:10.1016/j.atherosclerosis.2020.03.026

Cited by 6 publications

(5 citation statements)

References 37 publications

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“…Dyslipidemia is a key factor in the development of MI and its subsequent complications [ 42 ]. Clinical studies have found that increased TC and LDL-C, as well as decreased HDL-C were associated with elevated risk of MI, which was also appeared in our MI model [ 43 ]. Moreover, AST, Tn-I, MYO and BNP are sensitive markers of myocardial cell injury or death after MI [ 44 , 45 ].…”

Section: Discussionsupporting

confidence: 59%

Exosomes derived from human placental mesenchymal stem cells ameliorate myocardial infarction via anti-inflammation and restoring gut dysbiosis

Yang

Wang

Zhang

et al. 2022

BMC Cardiovasc Disord

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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.

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Section: Discussionsupporting

confidence: 59%

Exosomes derived from human placental mesenchymal stem cells ameliorate myocardial infarction via anti-inflammation and restoring gut dysbiosis

Yang

Wang

Zhang

et al. 2022

BMC Cardiovasc Disord

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“…Data were deprived from the Kailuan study, which is a prospective cohort study conducted in the Kailuan community in Tangshan, China. The detailed study design and procedures have been published previously [ 15 – 17 ]. Briefly, during June 2006 to October 2007, a total of 101,510 participants (81,110 men and 20,400 women, aged 18–98 years) were enrolled in the baseline survey and have completed questionnaires and health assessments biennially since 2006.…”

Section: Methodsmentioning

confidence: 99%

Insulin resistance mediates obesity-related risk of cardiovascular disease: a prospective cohort study

Tian

Chen

Wang

et al. 2022

Cardiovasc Diabetol

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Background The mechanisms linking obesity to cardiovascular disease (CVD) are still not clearly defined. Individuals who are overweight or obese often develop insulin resistance, mediation of the association between obesity and CVD through the insulin resistance seems plausible and has not been investigated. This study aimed to evaluate whether and to what extend the effect of general and central obesity on cardiovascular disease (CVD) is mediated by insulin resistance. Methods A total of 94,136 participants without CVD at baseline were recruited from the Kailuan study. Insulin resistance was evaluated by the triglyceride-glucose (TyG) index, calculating as ln [fasting triglyceride (mg/dL) × fasting glucose (mg/dL)/2]. Mediation analysis using a new 2-stage regression method for survival data proposed by Valeri and VanderWeele was to explore the mediating effects of the TyG index on the association between obesity and CVD. Results During a median follow-up of 13.01 years, we identified 7327 cases of CVD. Mediation analyses showed that 47.81% of the total association (hazard ratio [HR], 1.18; 95% confidence interval [CI], 1.12–1.24) between overweight and CVD was mediated through the TyG index (HR [indirect association], 1.07; 95% CI, 1.07–1.09), and the proportion mediated was 37.94% for general obesity. For central obesity, analysis by waist circumference, waist/hip, and waist/height categories yielded an attenuated proportion mediated of 32.01, 35.02, and 31.06% for obesity, taken normal weight as reference. Conclusions The association between obesity and CVD was mediated by TyG index, suggesting proper control of insulin resistance can be effective to reduce the effects of obesity on CVD.

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“…Lipid metabolism also undergoes significant changes in MI. Triglycerides, low-density lipoprotein cholesterol (LDL-C), nonhigh-density lipoprotein cholesterol (non-HDL-C), remnant cholesterol, and total cholesterol levels significantly increase after MI, while high-density lipoprotein cholesterol (HDL-C) decreases (198)(199)(200)(201). This lipid metabolism abnormality is closely associated with the development of coronary artery atherosclerosis and can be used to predict the risk of MI.…”

Section: Metabolomicsmentioning

confidence: 99%

From multi-omics approaches to personalized medicine in myocardial infarction

Zhan,

Tang,

et al. 2023

Front. Cardiovasc. Med.

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Myocardial infarction (MI) is a prevalent cardiovascular disease characterized by myocardial necrosis resulting from coronary artery ischemia and hypoxia, which can lead to severe complications such as arrhythmia, cardiac rupture, heart failure, and sudden death. Despite being a research hotspot, the etiological mechanism of MI remains unclear. The emergence and widespread use of omics technologies, including genomics, transcriptomics, proteomics, metabolomics, and other omics, have provided new opportunities for exploring the molecular mechanism of MI and identifying a large number of disease biomarkers. However, a single-omics approach has limitations in understanding the complex biological pathways of diseases. The multi-omics approach can reveal the interaction network among molecules at various levels and overcome the limitations of the single-omics approaches. This review focuses on the omics studies of MI, including genomics, epigenomics, transcriptomics, proteomics, metabolomics, and other omics. The exploration extended into the domain of multi-omics integrative analysis, accompanied by a compilation of diverse online resources, databases, and tools conducive to these investigations. Additionally, we discussed the role and prospects of multi-omics approaches in personalized medicine, highlighting the potential for improving diagnosis, treatment, and prognosis of MI.

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Association of changes in lipids with risk of myocardial infarction among people without lipid-lowering therapy

Cited by 6 publications

References 37 publications

Exosomes derived from human placental mesenchymal stem cells ameliorate myocardial infarction via anti-inflammation and restoring gut dysbiosis

Exosomes derived from human placental mesenchymal stem cells ameliorate myocardial infarction via anti-inflammation and restoring gut dysbiosis

Insulin resistance mediates obesity-related risk of cardiovascular disease: a prospective cohort study

From multi-omics approaches to personalized medicine in myocardial infarction

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