Role of Inflammatory Cytokines in Rheumatoid Arthritis and Development of Atherosclerosis: A Review

Bedeković, Dražen; Bošnjak, Ivica; Šarić, Sandra; Kirner, Damir; Novak, Srđan

doi:10.3390/medicina59091550

Cited by 12 publications

(8 citation statements)

References 150 publications

(373 reference statements)

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“…These cytokines not only participate in synovial development but also promote the activation of endothelial cells, leading to dysfunction and accelerating the progression of atherosclerosis through the modulation of inflammatory cascades 33,35 . Moreover, RA chronic inflammation also has procoagulant and prooxidant effects, increasing the expression of tissue factor adhesion molecules, reducing the synthesis of nitric oxide and thrombomodulin, and inducing nicotinamide adenine dinucleotide phosphate oxidase-mediated mechanisms 36,37 . This further leads to endothelial dysfunction and shifts the hemostatic balance of RA toward a prothrombotic state.…”

Section: Discussionmentioning

confidence: 99%

Causal Relationship between Rheumatoid Arthritis and Atherosclerosis Risk: A Mendelian Randomized Study

Liu,

Du,

Xie

et al. 2024

Preprint

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Objectives: Previous observational studies have revealed an association between rheumatoid arthritis (RA) and atherosclerosis (AS). However, observational studies are prone to bias due to potential confounding factors and reverse causality. Therefore, this study investigates the causal relationship between RA and AS risk using Mendelian randomization (MR). Methods: Genetic data related to RA and AS were sourced from the Integrative Epidemiology Unit Open-Genome-Wide Association Studies database and the seventh edition of the FinnGen Biobank gene database, respectively. The initial analysis employed the inverse variance weighted (IVW) method for the MR analysis, with other methods utilized as supplementary methods. To ensure the robustness and reliability of the conclusions, various sensitivity analyses were conducted. Results: The MR results indicate a positive causal relationship between genetically determined RA and the risk of coronary atherosclerosis(OR = 1.026, 95% CI: 1.004, 1.049, p = 0.179), peripheral atherosclerosis(OR = 1.072, 95% CI: 1.035, 1.111, p < 0.001), and atherosclerosis excluding coronary atherosclerosis, cerebral atherosclerosis, and PAD (ASE) (OR = 1.046, 95% CI: 1.015, 1.079, p = 0.004), while no significant causal relationship with cerebral AS was observed. The MR-Egger regression did not reveal any significant horizontal pleiotropy. Conclusion: This study elucidates the causal relationship between RA and various AS risks, highlighting the importance of actively detecting and intervening in RA for AS risk.

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Section: Discussionmentioning

confidence: 99%

Causal Relationship between Rheumatoid Arthritis and Atherosclerosis Risk: A Mendelian Randomized Study

Liu,

Du,

Xie

et al. 2024

Preprint

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show abstract

“…A subset of women with rheumatoid arthritis (RA), an autoimmune inflammatory disease, are also prone to developing cardiovascular disease [70][71][72][73]. Of interest is the fact that ~70% of female RA patients undergo a remission of their disease when pregnant and disease activity is also influenced by the menstrual cycle (reviewed in [74]).…”

Section: Variables and Factors Influencing Post-menopause Diseases An...mentioning

confidence: 99%

The Heterogeneity of Post-Menopausal Disease Risk: Could the Basis for Why Only Subsets of Females Are Affected Be Due to a Reversible Epigenetic Modification System Associated with Puberty, Menstrual Cycles, Pregnancy and Lactation, and, Ultimately, Menopause?

Hart

2024

IJMS

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For much of human evolution, the average lifespan was <40 years, due in part to disease, infant mortality, predators, food insecurity, and, for females, complications of childbirth. Thus, for much of evolution, many females did not reach the age of menopause (45–50 years of age) and it is mainly in the past several hundred years that the lifespan has been extended to >75 years, primarily due to public health advances, medical interventions, antibiotics, and nutrition. Therefore, the underlying biological mechanisms responsible for disease risk following menopause must have evolved during the complex processes leading to Homo sapiens to serve functions in the pre-menopausal state. Furthermore, as a primary function for the survival of the species is effective reproduction, it is likely that most of the advantages of having such post-menopausal risks relate to reproduction and the ability to address environmental stresses. This opinion/perspective will be discussed in the context of how such post-menopausal risks could enhance reproduction, with improved survival of offspring, and perhaps why such risks are preserved. Not all post-menopausal females exhibit risk for this set of diseases, and those who do develop such diseases do not have all of the conditions. The diseases of the post-menopausal state do not operate as a unified complex, but as independent variables, with the potential for some overlap. The how and why there would be such heterogeneity if the risk factors serve essential functions during the reproductive years is also discussed and the concept of sets of reversible epigenetic changes associated with puberty, pregnancy, and lactation is offered to explain the observations regarding the distribution of post-menopausal conditions and their potential roles in reproduction. While the involvement of an epigenetic system with a dynamic “modification-demodification-remodification” paradigm contributing to disease risk is a hypothesis at this point, validation of it could lead to a better understanding of post-menopausal disease risk in the context of reproduction with commonalities may also lead to future improved interventions to control such risk after menopause.

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“…Studies have shown that TNF-α inhibition significantly improves vascular function in RA patients [ 21 ]. Inflammatory cytokines, immune cells and many others play vital roles in both RA and the development of AS [ 22 , 23 ]. Latest research indicates a positive association between genetic predisposition to RA and high risk of coronary AS.…”

Section: Introductionmentioning

confidence: 99%

Detection of common pathogenesis of rheumatoid arthritis and atherosclerosis via microarray data analysis

Xu,

Xie,

et al. 2024

Heliyon

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Role of Inflammatory Cytokines in Rheumatoid Arthritis and Development of Atherosclerosis: A Review

Cited by 12 publications

References 150 publications

Causal Relationship between Rheumatoid Arthritis and Atherosclerosis Risk: A Mendelian Randomized Study

Causal Relationship between Rheumatoid Arthritis and Atherosclerosis Risk: A Mendelian Randomized Study

The Heterogeneity of Post-Menopausal Disease Risk: Could the Basis for Why Only Subsets of Females Are Affected Be Due to a Reversible Epigenetic Modification System Associated with Puberty, Menstrual Cycles, Pregnancy and Lactation, and, Ultimately, Menopause?

Detection of common pathogenesis of rheumatoid arthritis and atherosclerosis via microarray data analysis

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