Зміни Ліпідного Обміну У Хворих На Ревматоїдний Артрит Із Супутньою Артеріальною Гіпертензією, Абдомінальним Ожирінням Та Цукровим Діабетом Типу 2 Залежно Від Поліморфізму Гена T-786с Ендотеліальної Оксиду Азоту Синтази

Bukach, O.; Федів, О. І.; Sydorchuk, Larysa

doi:10.22141/2224-0721.13.1.2017.96762

Cited by 2 publications

(1 citation statement)

References 11 publications

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“…In addition, most variants outside the HLA region with a positive correlation to the elevated cardiovascular risk among rheumatoid arthritis patients on the basis of this review, are connected to genes encoding for proteins of cells and molecules of the immune system, including the tumor necrosis factor (TNF) superfamily genes, cytokines and related genes, chemokines, or adipokines [ 1 ▪ ]. Furthermore, correlations have also been found with variants of genes involved in nitric oxide synthesis [ 11 ] and vitamin D levels [ 12 ]. Finally, there are some additional exciting potential associations with other, seemingly unrelated genes, such as MTHFR , important in the homocysteine plasma level homeostasis [ 13 ].…”

Section: Genetic Background Of Cardiovascular Complications In Autoimmentioning

confidence: 99%

Mechanisms of vascular comorbidity in autoimmune diseases

Nagy

Nemeth²,

Buzás

2018

Current Opinion in Rheumatology

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Purpose of reviewPersuasive statistics support the clinical observation that because of cardiovascular comorbidities patients with inflammatory joint disease die significantly earlier despite anti-inflammatory therapy.Recent findingsThe reason for this earlier death is multifactorial and involves a combination of a complex genetic background, environmental influences, classical cardiovascular risk factors and the impact of anti-inflammatory therapy. We will describe the importance of several new mechanisms, especially the diverse intercellular communication routes including extracellular vesicles and microRNAs that support the development of cardiovascular comorbidities.SummaryThe aim of this review is to give an updated overview about the known risk factors in the development of cardiovascular comorbidities with the latest insights about their mechanism of action. Furthermore, the impact of newly identified risk factors and significance will be discussed.

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Section: Genetic Background Of Cardiovascular Complications In Autoimmentioning

confidence: 99%

Mechanisms of vascular comorbidity in autoimmune diseases

Nagy

Nemeth²,

Buzás

2018

Current Opinion in Rheumatology

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Metabolic Enzyme Triosephosphate Isomerase 1 and Nicotinamide Phosphoribosyltransferase, Two Independent Inflammatory Indicators in Rheumatoid Arthritis: Evidences From Collagen-Induced Arthritis and Clinical Samples

Lei

Tao

et al. 2022

Front. Immunol.

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Metabolic intervention is a novel anti-rheumatic approach. The glycolytic regulator NAMPT has been identified as a therapeutic target of rheumatoid arthritis (RA), while other metabolic regulators coordinating NAMPT to perpetuate inflammation are yet to be investigated. We continuously monitored and validated expression changes of Nampt and inflammatory indicators in peripheral while blood cells from rats with collagen-induced arthritis (CIA). Gene transcriptional profiles of Nampt+ and Nampt++ samples from identical CIA rats were compared by RNA-sequencing. Observed gene expression changes were validated in another batch of CIA rats, and typical metabolic regulators with persistent changes during inflammatory courses were further investigated in human subjects. According to expression differences of identified genes, RA patients were assigned into different subsets. Clinical manifestation and cytokine profiles among them were compared afterwards. Nampt overexpression typically occurred in CIA rats during early stages, when iNos and Il-1β started to be up-regulated. Among differentially expressed genes between Nampt+ and Nampt++ CIA rat samples, changes of Tpi1, the only glycolytic enzyme identified were sustained in the aftermath of acute inflammation. Similar to NAMPT, TPI1 expression in RA patients was higher than general population, which was synchronized with increase in RFn as well as inflammatory monocytes-related cytokines like Eotaxin. Meanwhile, RANTES levels were relatively low when NAMPT and TPI1 were overexpressed. Reciprocal interactions between TPI1 and HIF-1α were observed. HIF-1α promoted TPI1 expression, while TPI1 co-localized with HIF-1α in nucleus of inflammatory monocytes. In short, although NAMPT and TPI1 dominate different stages of CIA, they similarly provoke monocyte-mediated inflammation.

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Cited by 2 publications

References 11 publications

Mechanisms of vascular comorbidity in autoimmune diseases

Mechanisms of vascular comorbidity in autoimmune diseases

Metabolic Enzyme Triosephosphate Isomerase 1 and Nicotinamide Phosphoribosyltransferase, Two Independent Inflammatory Indicators in Rheumatoid Arthritis: Evidences From Collagen-Induced Arthritis and Clinical Samples

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