Selected Atherosclerosis-Related Diseases May Differentially Affect the Relationship between Plasma Advanced Glycation End Products, Receptor sRAGE, and Uric Acid

Gryszczyńska, Bogna; Budzyń, Magdalena; Formanowicz, Dorota; Wanic-Kossowska, Maria; Formanowicz, Piotr; Majewski, Wacław; Iskra, Maria; Kasprzak, Magdalena Paulina

doi:10.3390/jcm9051416

Cited by 7 publications

(10 citation statements)

References 48 publications

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“…As a result, an increase in the concentration of ADMA, which inhibits the formation of NO, is observed [184]. The increase in the concentration of oxidative stress markers, such as MDA, ox-LDL, and the increase in ADMA concentration correlates with the degree of endothelial damage in the course of CKD [184][185][186].…”

Section: Disordered No Metabolismmentioning

confidence: 99%

Chronic Kidney Disease as Oxidative Stress- and Inflammatory-Mediated Cardiovascular Disease

Podkowińska¹,

2020

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Generating reactive oxygen species (ROS) is necessary for both physiology and pathology. An imbalance between endogenous oxidants and antioxidants causes oxidative stress, contributing to vascular dysfunction. The ROS-induced activation of transcription factors and proinflammatory genes increases inflammation. This phenomenon is of crucial importance in patients with chronic kidney disease (CKD), because atherosclerosis is one of the critical factors of their cardiovascular disease (CVD) and increased mortality. The effect of ROS disrupts the excretory function of each section of the nephron. It prevents the maintenance of intra-systemic homeostasis and leads to the accumulation of metabolic products. Renal regulatory mechanisms, such as tubular glomerular feedback, myogenic reflex in the supplying arteriole, and the renin–angiotensin–aldosterone system, are also affected. It makes it impossible for the kidney to compensate for water–electrolyte and acid–base disturbances, which progress further in the mechanism of positive feedback, leading to a further intensification of oxidative stress. As a result, the progression of CKD is observed, with a spectrum of complications such as malnutrition, calcium phosphate abnormalities, atherosclerosis, and anemia. This review aimed to show the role of oxidative stress and inflammation in renal impairment, with a particular emphasis on its influence on the most common disturbances that accompany CKD.

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Section: Disordered No Metabolismmentioning

confidence: 99%

Chronic Kidney Disease as Oxidative Stress- and Inflammatory-Mediated Cardiovascular Disease

Podkowińska¹,

2020

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“…Increased oxidation and reduced clearance of AGE-modified LDL may contribute to CKD patients’ increased risk of atherosclerosis [ 96 ]. We give an overview of human studies investigating the role of AGEs and sRAGE in atherosclerosis in Table 4 [ 62 , 97 , 98 , 99 , 100 , 101 , 102 , 103 ].…”

Section: Atherosclerosismentioning

confidence: 99%

“…The increase in AGE levels might be explained by increased oxidative stress and a loss of kidney function. The underlying pathophysiological process may be based on growing protein stiffness caused by protein cross-linking, cytokine, and enhanced adhesion molecule expression [ 100 ]. AGEs have been detected in the atherosclerotic plaques of patients with CKD [ 101 ].…”

Section: Atherosclerosismentioning

confidence: 99%

“…A positive association was found between the level of AGEs and the concentration of sRAGE. AGEs induce the production of sRAGE, showing an increase in the production of scavenging receptors to defend against growing oxidative stress in CKD [ 100 ]. The amount of sRAGE in CKD-G5D patients was considerably higher than in CKD stage 3–4 patients, suggesting that it may be a protective mechanism against increasing oxidative stress and inflammation [ 62 ].…”

Section: Atherosclerosismentioning

confidence: 99%

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The Role of Advanced Glycation End Products and Its Soluble Receptor in Kidney Diseases

Steenbeke

Speeckaert

Desmedt

et al. 2022

IJMS

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Patients with chronic kidney disease (CKD) are more prone to oxidative stress and chronic inflammation, which may lead to an increase in the synthesis of advanced glycation end products (AGEs). Because AGEs are mostly removed by healthy kidneys, AGE accumulation is a result of both increased production and decreased kidney clearance. On the other hand, AGEs may potentially hasten decreasing kidney function in CKD patients, and are independently related to all-cause mortality. They are one of the non-traditional risk factors that play a significant role in the underlying processes that lead to excessive cardiovascular disease in CKD patients. When AGEs interact with their cell-bound receptor (RAGE), cell dysfunction is initiated by activating nuclear factor kappa-B (NF-κB), increasing the production and release of inflammatory cytokines. Alterations in the AGE-RAGE system have been related to the development of several chronic kidney diseases. Soluble RAGE (sRAGE) is a decoy receptor that suppresses membrane-bound RAGE activation and AGE-RAGE-related toxicity. sRAGE, and more specifically, the AGE/sRAGE ratio, may be promising tools for predicting the prognosis of kidney diseases. In the present review, we discuss the potential role of AGEs and sRAGE as biomarkers in different kidney pathologies.

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“…Aortic aneurysms and aortic dissection are among the atherosclerosis-related acute aortic syndromes [ 1 , 2 , 3 ]. An aneurysm is a condition in which a part of the wall of the aorta circumferentially or locally enlarges or protrudes [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

Preventive Effects of Quercetin against the Onset of Atherosclerosis-Related Acute Aortic Syndromes in Mice

Kondo

Izawa‐Ishizawa

Goda

et al. 2020

IJMS

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Atherosclerosis-related acute aortic syndromes, such as aortic aneurysms or aortic dissection are life-threatening diseases. Since they develop suddenly and progress rapidly, the establishment of preventive strategies is urgently needed. Quercetin, a flavonoid abundant in various vegetables and fruits, is suggested to reduce the risk of cardiovascular disease. Therefore, in this study, the preventive effect of quercetin was evaluated using a mouse model of aortic aneurysm and dissection. The model was established by administering angiotensin II (Ang II) and β-aminopropionitrile (BAPN), a lysyl oxidase inhibitor, to mice to induce hypertension and degeneration of the elastic lamina, which would eventually result in the onset of an aortic aneurysm. Ang II, BAPN, and a nitric oxide synthase inhibitor was administered to induce aortic dissection via endothelial dysfunction. Quercetin (60 mg/kg/day) was administered 2 weeks before inducing aortic diseases by the end of the experiments (8 weeks in the aneurysm model, 6 weeks in the dissection model). It was found to reduce the incidence of aneurysm (from 72 to 45%), dissection (from 17 to 10%), and rupture (from 33 to 15%) in mice. Elastin degradation was ameliorated in the quercetin-treated mice compared to that in the mice without quercetin treatment (degradation score 2.9 ± 0.3 vs 2.2 ± 0.2). Furthermore, quercetin suppressed the expression of vascular cell adhesion molecule-1, macrophage infiltration, and pro-matrix metalloproteinase-9 activity. Our results suggest that quercetin might prevent the onset of atherosclerosis-related acute aortic syndromes through its anti-inflammatory and endothelial cell-protective effects.

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Selected Atherosclerosis-Related Diseases May Differentially Affect the Relationship between Plasma Advanced Glycation End Products, Receptor sRAGE, and Uric Acid

Cited by 7 publications

References 48 publications

Chronic Kidney Disease as Oxidative Stress- and Inflammatory-Mediated Cardiovascular Disease

Chronic Kidney Disease as Oxidative Stress- and Inflammatory-Mediated Cardiovascular Disease

The Role of Advanced Glycation End Products and Its Soluble Receptor in Kidney Diseases

Preventive Effects of Quercetin against the Onset of Atherosclerosis-Related Acute Aortic Syndromes in Mice

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