Association of polymorphism 4a/4b and 4b/4b in endothelial nitric oxide synthase gene and markers of endothelial dysfunction in patients with chronic heart failure

Полунина, Е. А.; Воронина, Л. П.; Севостьянова, И В; Полунина, О. С.; Тарасочкина, Д. С.

doi:10.18087/cardio.2448

Cited by 5 publications

(2 citation statements)

References 8 publications

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“…Vascular endothelial cells (VECs), the inner lining of blood vessels, serve as an anti-thrombotic and anti-inflammatory barrier and are critically involved in the maintenance of vascular homeostasis, regulating vascular movement and participating in life activation 2 . Endothelial cell dysfunction (ECD) is the fundamental of cardiovascular diseases 3 . Endothelial dysfunction leads to endothelium inflammation, and further impairs endothelial integrity.…”

Section: Introductionmentioning

confidence: 99%

Aspirin alleviates endothelial gap junction dysfunction through inhibition of NLRP3 inflammasome activation in LPS-induced vascular injury

Xing

et al. 2019

Acta Pharmaceutica Sinica B

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The loss of endothelial connective integrity and endothelial barrier dysfunction can lead to increased vascular injury, which is related to the activation of endothelial inflammasomes. There are evidences that low concentrations of aspirin can effectively prevent cardiovascular diseases. We hypothesized that low-dose aspirin could ameliorate endothelial injury by inhibiting the activation of NLRP3 inflammasomes and ultimately prevent cardiovascular diseases. Microvascular endothelial cells were stimulated by lipopolysaccharide (2 μg/mL) and administrated by 0.1–2 mmol/L aspirin. The wild type mice were stimulated with LPS (100 μg/kg/day), and 1 h later treated with aspirin (12.5, 62.5, or 125 mg/kg/day) and dexamethasone (0.0182 mg/kg/day) for 7 days. Plasma and heart were harvested for measurement of ELISA and immunofluorescence analyses. We found that aspirin could inhibit NLRP3 inflammasome formation and activation in vitro in dose-dependent manner and has correlation between the NLRP3 inflammasome and the ROS/TXNIP pathway. We also found that low-concentration aspirin could inhibit the formation and activation of NLRP3 inflammasome and restore the expression of the endothelial tight junction protein zonula occludens-1/2 (ZO1/2). We assume that aspirin can ameliorate the endothelial layer dysfunction by suppressing the activation of NLRP3 inflammasome.

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Section: Introductionmentioning

confidence: 99%

Aspirin alleviates endothelial gap junction dysfunction through inhibition of NLRP3 inflammasome activation in LPS-induced vascular injury

Xing

et al. 2019

Acta Pharmaceutica Sinica B

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“…As an important aspect of VR, vascular remodeling is often caused by angiogenesis and endothelial damage, which involves VECs (Alexandru et al, 2020; Lother et al, 2019; Segers et al, 2018). As a barrier against inflammation and thrombosis, VECs play an important role in maintaining the homeostasis of the vascular environment (Polunina et al, 2018; X. Zhang et al, 2018). VEC dysfunction promotes VR by affecting angiogenesis, reducing capillary density, and promoting atherosclerosis (AS), thereby affecting the balance of oxygen supply and energy uptake of the heart.…”

Section: Regulatory Effects Of the Nlrp3 Inflammasome In Primary Cells During Vrmentioning

confidence: 99%

The NLRP3 inflammasome: Multiple activation pathways and its role in primary cells during ventricular remodeling

Yan

Yang

et al. 2021

Journal Cellular Physiology

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Inflammasomes are a group of multiprotein signaling complexes located in the cytoplasm. Several inflammasomes have been identified, including NLRP1, NLRP2, NLRP3, AIM2, and NLRC4. Among them, NLRP3 was investigated in most detail, and it was reported that it can be activated by many different stimuli. Increased NLRP3 protein expression and inflammasome assembly lead to caspase‐1 mediated maturation and release of IL‐1β, which triggers inflammation and pyroptosis. The activation of the NLRP3 inflammasome has been widely reported in studies of tumors and neurological diseases, but relatively few studies on the cardiovascular system. Ventricular remodeling (VR) is an important factor contributing to heart failure (HF) after myocardial infarction (MI). Consequently, delaying VR is of great significance for improving heart function. Studies have shown that the NLRP3 inflammasome plays an essential role in the process of VR. Here, we reviewed the latest studies on the activation pathway of the NLRP3 inflammasome, focusing on the effects of the NLRP3 inflammasome in primary cells during VR, and finally discuss future research directions in this field.

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Relationship of gene polymorphism with the nature of target organ damage in patients with arterial hypertension

Drobotya

Arutyunyan²,

Пироженко

et al. 2020

jour

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Objective: to assess the relationship of polymorphism of the main genes involved in the pathogenesis of arterial hypertension (AH) with indicators reflecting the state of target organs in the group of patients with arterial hypertension.Material and methods: we examined 100 patients with arterial hypertension who underwent standard diagnostic procedures, as well as molecular genetic research.Results: in patients with arterial hypertension statistically significant associations of AGTR2, GNB3, and NOS3 gene polymorphism with left ventricular hypertrophy, CYP11B2 and NOS3 gene polymorphism with left ventricular diastolic dysfunction, and NOS3 gene polymorphism with increased vascular wall stiffness were found (p < 0.05).Conclusions: the results of the study indicate that patients with arterial hypertension are a genetically heterogeneous group in terms of the relationship of specific gene polymorphism with indicators that characterize the state of target organs. The use of genetic approaches is promising for early screening of patients with arterial hypertension, belonging to the high-risk group, in order to ensure timely and effective organoprotection.

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Association of polymorphism 4a/4b and 4b/4b in endothelial nitric oxide synthase gene and markers of endothelial dysfunction in patients with chronic heart failure

Cited by 5 publications

References 8 publications

Aspirin alleviates endothelial gap junction dysfunction through inhibition of NLRP3 inflammasome activation in LPS-induced vascular injury

Aspirin alleviates endothelial gap junction dysfunction through inhibition of NLRP3 inflammasome activation in LPS-induced vascular injury

The NLRP3 inflammasome: Multiple activation pathways and its role in primary cells during ventricular remodeling

Relationship of gene polymorphism with the nature of target organ damage in patients with arterial hypertension

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