Dataset Information

The Association between Educational Level and Cardiovascular and Cerebrovascular Diseases within the EPICOR Study: New Evidence for an Old Inequality Problem.

ABSTRACT:

Background

A consistent association has been reported between low socioeconomic status (SES) and cardiovascular events (CE), whereas the association between SES and cerebrovascular events (CBVD) is less clear. The aim of this study was to investigate the association between SES (measured using education) and CE/CBVD in a cohort study, as well as to investigate lifestyle and clinical risk factors, to help to clarify the mechanisms by which SES influences CE/CBVD.

Material and methods

We searched for diagnoses of CE and CBVD in the clinical records of 47,749 members of the EPICOR cohort (average follow-up time: 11 years). SES was determined by the relative index of inequality (RII).

Results

A total of 1,156 CE and 468 CBVD were found in the clinical records. An increased risk of CE was observed in the crude Cox model for the third tertile of RII compared to the first tertile (hazard ratio [HR] = 1.39; 95% confidence interval [CI] 1.21-1.61). The increased risk persisted after adjustment for lifestyle risk factors (HR = 1.19; 95%CI 1.02-1.38), clinical risk factors (HR = 1.35; 95%CI 1.17-1.56), and after full adjustment (HR = 1.17; 95%CI 1.01-1.37). Structural equation model showed that lifestyle rather than clinical risk factors are involved in the mechanisms by which education influences CE. No significant association was found between education and CBVD. A strong relationship was observed between education and diabetes at baseline.

Conclusion

The most important burden of inequality in CE incidence in Italy is due to lifestyle risk factors.

SUBMITTER: Ricceri F

PROVIDER: S-EPMC5053474 | biostudies-literature | 2016

REPOSITORIES: biostudies-literature

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Publications

The Association between Educational Level and Cardiovascular and Cerebrovascular Diseases within the EPICOR Study: New Evidence for an Old Inequality Problem.

Ricceri Fulvio F Sacerdote Carlotta C Giraudo Maria Teresa MT Fasanelli Francesca F Lenzo Giulia G Galli Matteo M Sieri Sabina S Pala Valeria V Masala Giovanna G Bendinelli Benedetta B Tumino Rosario R Frasca Graziella G Chiodini Paolo P Mattiello Amalia A Panico Salvatore S

PloS one 20161006 10

<h4>Background</h4>A consistent association has been reported between low socioeconomic status (SES) and cardiovascular events (CE), whereas the association between SES and cerebrovascular events (CBVD) is less clear. The aim of this study was to investigate the association between SES (measured using education) and CE/CBVD in a cohort study, as well as to investigate lifestyle and clinical risk factors, to help to clarify the mechanisms by which SES influences CE/CBVD.<h4>Material and methods</ ...[more]

PMID: 27711245

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Project description:Background and Aims: Atherosclerosis, a major contributor to cardiovascular and cerebrovascular diseases, remains a leading cause of global mortality and morbidity. This study focuses on the role of chemokine-like receptor 1 (CMKLR1) in VSMCs and its potential impact on atherosclerotic plaque formation and remodelling. Methods: Cmklr1-/-Apoe-/- mice, generated using CRISPR/Cas9 technology, were fed a high-fat western diet for 16 weeks to model atherosclerosis. Primary VSMCs were isolated from Cmklr1-/- and Cmklr1+/+ mice for in vitro experiments. Cell viability, senescence-associated β-galactosidase staining, and RNA interference were performed to assess the effect of CMKLR1 deficiency on VSMCs. Various assays, including flow cytometry, immunocytochemistry, and RNA-seq analysis, were employed to investigate the molecular mechanisms and downstream signals associated with CMKLR1 deficiency. Results: CMKLR1 deficiency was found to disrupt the cell cycle, leading to VSMC senescence both in vitro and in vivo. Cmklr1-/-Apoe-/- mice exhibited increased atherosclerotic plaque burden, emphasizing the role of CMKLR1 in plaque stability. Transcriptome analysis revealed significant changes in cellular components and biological processes, with a particular impact on the extracellular matrix and cellular response to stimulus. The TGFβ signalling pathway emerged as a potential downstream target of CMKLR1, affecting VSMC differentiation, vessel development, and extracellular matrix synthesis. The deficiency of CMKLR1 led to a reduction in TGFβ1 expression and downstream molecule SM22α, influencing plaque composition and stability. Conclusion: This study demonstrates that CMKLR1 deficiency promotes VSMC senescence and exacerbates atherosclerosis. The disrupted TGFβ signalling pathway, identified as a potential molecular mechanism, provides insights into the complex regulatory network associated with CMKLR1 in atherosclerotic plaque formation and remodelling. These findings highlight the importance of CMKLR1 in atherosclerosis and its potential as a therapeutic target for plaque stability.

Dataset Information

The Association between Educational Level and Cardiovascular and Cerebrovascular Diseases within the EPICOR Study: New Evidence for an Old Inequality Problem.

Background

Material and methods

Results

Conclusion

Publications

The Association between Educational Level and Cardiovascular and Cerebrovascular Diseases within the EPICOR Study: New Evidence for an Old Inequality Problem.

Similar Datasets

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