scholarly journals Vascular Calcification—New Insights into Its Mechanism

2020 ◽  
Vol 21 (8) ◽  
pp. 2685 ◽  
Author(s):  
Sun Joo Lee ◽  
In-Kyu Lee ◽  
Jae-Han Jeon
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Vascular Calcification ◽  
Mitochondrial Oxidative Stress ◽  
The Past ◽  
Defensive Mechanisms ◽  
Osteogenic Signaling ◽  
Multiple Signaling ◽  
Medial Calcification

Vascular calcification (VC), which is categorized by intimal and medial calcification, depending on the site(s) involved within the vessel, is closely related to cardiovascular disease. Specifically, medial calcification is prevalent in certain medical situations, including chronic kidney disease and diabetes. The past few decades have seen extensive research into VC, revealing that the mechanism of VC is not merely a consequence of a high-phosphorous and -calcium milieu, but also occurs via delicate and well-organized biologic processes, including an imbalance between osteochondrogenic signaling and anticalcific events. In addition to traditionally established osteogenic signaling, dysfunctional calcium homeostasis is prerequisite in the development of VC. Moreover, loss of defensive mechanisms, by microorganelle dysfunction, including hyper-fragmented mitochondria, mitochondrial oxidative stress, defective autophagy or mitophagy, and endoplasmic reticulum (ER) stress, may all contribute to VC. To facilitate the understanding of vascular calcification, across any number of bioscientific disciplines, we provide this review of a detailed updated molecular mechanism of VC. This encompasses a vascular smooth muscle phenotypic of osteogenic differentiation, and multiple signaling pathways of VC induction, including the roles of inflammation and cellular microorganelle genesis.

scholarly journals Bibliometric and Visual Analysis of Vascular Calcification Research

2021 ◽  
Vol 12 ◽  
Author(s):  
Qian Dong ◽  
Qingchun Liang ◽  
Ying Chen ◽  
Jinhe Li ◽  
Lihe Lu ◽  
...  
Keyword(s):  
United States ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Visual Analysis ◽  
The United States ◽  
Signal Pathways ◽  
Growth Trend ◽  
The Past

Background: Extensive studies related to vascular calcification (VC) were conducted in recent years. However, no bibliometric analysis has systematically investigated this topic. Our study aimed to determine the hotspots and frontiers of VC research in the past decade and provide a reference for future scientific research directions and decision-making in the VC field.Methods: VC studies were acquired from the Web of Science Core Collection. Bibliometric and visual analyses were performed using CiteSpace, VOSviewer, and Microsoft Excel software.Results: A total of 8,238 English articles on VC research published in 2011–2020 were obtained. In the past decade, annual publications and citations showed a significant growth trend, especially in 2018–2020. The most productive country, institution, journal and author are the United States, the University of California System, PLOS ONE, and Budoff MJ, respectively. The most frequently cited country, journal, and author are the United States, Journal of the American College of Cardiology, and Floege J, respectively. “Vascular calcification,” “atherosclerosis,” “chronic kidney disease,” and “cardiovascular disease” are the primary keywords. The burst keywords “revascularization,” “calciprotein particle,” “microRNA,” and “microcalcification” are speculated to be the research frontiers.Conclusion: The main research hotspots in the VC field are the molecular mechanisms and prognosis of VC in patients with chronic kidney disease or cardiovascular disease. In addition, endovascular therapy and the development of new drugs targeting signal pathways for VC will become the focus of future research. Moreover, non-coding RNAs related to the diagnosis and treatment of VC are great research prospects.

scholarly journals NOX4 NADPH Oxidase-Dependent Mitochondrial Oxidative Stress in Aging-Associated Cardiovascular Disease

2015 ◽  
Vol 23 (18) ◽  
pp. 1389-1409 ◽  
Author(s):  
Aleksandr E. Vendrov ◽  
Kimberly C. Vendrov ◽  
Alberto Smith ◽  
Jinling Yuan ◽  
Arihiro Sumida ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Nadph Oxidase ◽  
Mitochondrial Oxidative Stress

scholarly journals The Essential Element Manganese, Oxidative Stress, and Metabolic Diseases: Links and Interactions

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Longman Li ◽  
Xiaobo Yang
Keyword(s):  
Oxidative Stress ◽  
Metabolic Diseases ◽  
Essential Element ◽  
Ros Generation ◽  
Oxygen Species ◽  
Mitochondrial Oxidative Stress ◽  
Nonalcoholic Fatty Liver ◽  
The Past ◽  
The Relationship

Manganese (Mn) is an essential element that is involved in the synthesis and activation of many enzymes and in the regulation of the metabolism of glucose and lipids in humans. In addition, Mn is one of the required components for Mn superoxide dismutase (MnSOD) that is mainly responsible for scavenging reactive oxygen species (ROS) in mitochondrial oxidative stress. Both Mn deficiency and intoxication are associated with adverse metabolic and neuropsychiatric effects. Over the past few decades, the prevalence of metabolic diseases, including type 2 diabetes mellitus (T2MD), obesity, insulin resistance, atherosclerosis, hyperlipidemia, nonalcoholic fatty liver disease (NAFLD), and hepatic steatosis, has increased dramatically. Previous studies have found that ROS generation, oxidative stress, and inflammation are critical for the pathogenesis of metabolic diseases. In addition, deficiency in dietary Mn as well as excessive Mn exposure could increase ROS generation and result in further oxidative stress. However, the relationship between Mn and metabolic diseases is not clear. In this review, we provide insights into the role Mn plays in the prevention and development of metabolic diseases.

scholarly journals New Insights into the Roles of Monocytes/Macrophages in Cardiovascular Calcification Associated with Chronic Kidney Disease

Toxins ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 529 ◽  
Author(s):  
Hénaut ◽  
Candellier ◽  
Boudot ◽  
Grissi ◽  
Mentaverri ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Cellular Interactions ◽  
Valvular Interstitial Cells ◽  
Macrophage Subset ◽  
And Oxidative Stress ◽  
Pro Inflammatory Cytokines ◽  
Valvular Cells

Cardiovascular disease (CVD) is an important cause of death in patients with chronic kidney disease (CKD), and cardiovascular calcification (CVC) is one of the strongest predictors of CVD in this population. Cardiovascular calcification results from complex cellular interactions involving the endothelium, vascular/valvular cells (i.e., vascular smooth muscle cells, valvular interstitial cells and resident fibroblasts), and monocyte-derived macrophages. Indeed, the production of pro-inflammatory cytokines and oxidative stress by monocyte-derived macrophages is responsible for the osteogenic transformation and mineralization of vascular/valvular cells. However, monocytes/macrophages show the ability to modify their phenotype, and consequently their functions, when facing environmental modifications. This plasticity complicates efforts to understand the pathogenesis of CVC—particularly in a CKD setting, where both uraemic toxins and CKD treatment may affect monocyte/macrophage functions and thereby influence CVC. Here, we review (i) the mechanisms by which each monocyte/macrophage subset either promotes or prevents CVC, and (ii) how both uraemic toxins and CKD therapies might affect these monocyte/macrophage functions.

scholarly journals Chronic Kidney Disease and Disproportionally Increased Cardiovascular Damage: Does Oxidative Stress Explain the Burden?

2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Anila Duni ◽  
Vassilios Liakopoulos ◽  
Karolos-Pavlos Rapsomanikis ◽  
Evangelia Dounousi
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Left Ventricular ◽  
Antioxidant Defenses ◽  
Pon1 Activity ◽  
Pathophysiological Mechanism ◽  
Ros Production ◽  
Cardiovascular Damage

Chronic kidney disease (CKD) patients are among the groups at the highest risk for cardiovascular disease and significantly shortened remaining lifespan. CKD enhances oxidative stress in the organism with ensuing cardiovascular damage. Oxidative stress in uremia is the consequence of higher reactive oxygen species (ROS) production, whereas attenuated clearance of pro-oxidant substances and impaired antioxidant defenses play a complementary role. The pathophysiological mechanism underlying the increased ROS production in CKD is at least partly mediated by upregulation of the intrarenal angiotensin system. Enhanced oxidative stress in the setting of the uremic milieu promotes enzymatic modification of circulating lipids and lipoproteins, protein carbamylation, endothelial dysfunction via disruption of nitric oxide (NO) pathways, and activation of inflammation, thus accelerating atherosclerosis. Left ventricular hypertrophy (LVH) and heart failure are hallmarks of CKD. NADPH oxidase activation, xanthine oxidase, mitochondrial dysfunction, and NO-ROS are the main oxidative pathways leading to LVH and the cardiorenal syndrome. Finally, a subset of antioxidant enzymes, the paraoxonases (PON), deserves special attention due to abundant clinical evidence accumulated regarding reduced serum PON1 activity in CKD as a contributor to the increased burden of cardiovascular disease. Future, meticulously designed studies are needed to assess the effects of antioxidant therapy on patients with CKD.

scholarly journals Epigenetics: Pharmacology and Modification Mechanisms Involved in Cardiac, Hepatic and Renal Disease

2020 ◽  
Vol 10 (4) ◽  
pp. 260-266
Author(s):  
Sagar. S. Waghmare ◽  
O.G. Bhusnure ◽  
M. R. Mali ◽  
S.T. Mule
Keyword(s):  
Gene Expression ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Dna Methylation ◽  
Kidney Disease ◽  
Epigenetic Modification ◽  
Hepatic Disease ◽  
Human Diseases ◽  
Future Perspective ◽  
The Past

For a long time scientists have tried to describe disorders are due to genetic as well as environmental factors. In the past few years, revolution in technology that has made it possible to decipher the human genome. Epigenetics explains the capability gene expression regulation without modifying the genetic sequence. Epigenetic mechanisms are rooted changes in molecules, or nuclear characteristics that can alter gene expression without altering the sequences of DNA, i.e. DNA methylation, histone modification, and non-coding RNAs. Learning of the fundamental epigenetic modification allowing gene expression as well as cellular phenotype are advanced that novel insights into the epigenetic control of cardiovascular disease, hepatic disease, as well as chronic kidney disease are now emerging. From a half of century ago, in human disease the role of epigenetics has been considered. This subject has attracted many interests in the past decade, especially in complicated diseases like cardiovascular disease, hepatic disease as well as chronic kidney disease. This review first illustrates the history and classification of epigenetic modifications and the factors (i.e. genetic, environment, dietary, thought process and lifestyle) affecting to the epigenetics mechanisms. Likewise, the epigenetics role in human diseases is think out by targeting on some diseases and at the end, we have given the future perspective of this field. This review article provides concepts with some examples to describe a broad view of distinct aspects of epigenetics in biology and human diseases. Keywords: - Epigenetics, DNA methylation, Histone modifications, microRNAs and Gene expression and Disease.

Abstract 17021: A Novel Human Relaxin Receptor Agonist, ML290, Attenuates Atherosclerosis- and Chronic Kidney Disease-Induced Vascular Calcification in Mice

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Hooi Hooi Ng ◽  
Daniela Medina ◽  
Alexander I Agoulnik ◽  
Joshua Hutcheson
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Therapeutic Potential ◽  
Superoxide Production ◽  
Scaffolding Protein ◽  
Cardiovascular Morbidity And Mortality ◽  
Relaxin Receptor ◽  
Medial Calcification

Introduction: Vascular calcification is the most significant predictor of cardiovascular morbidity and mortality, but therapeutic options are unavailable. Relaxin has emerged as a vasoprotective molecule, but several drawbacks prevent therapeutic translation. Targeting the relaxin receptor, RXFP1, is safe and well-tolerated in animal models of vascular disease and humans. We identified a biased allosteric agonist of human RXFP1, ML290, and aimed to test the hypothesis that ML290 arrests the progression of vascular calcification in mouse models of atherosclerosis and chronic kidney disease (CKD). Methods and Results: Recurrent treatment with ML290 significantly prevented ( P = 0.0422, n = 8) and reversed ( P = 0.0489, n = 6) atherosclerotic calcification in humanized ( hRXFP1/hRXFP1 ) Apoe -/- mice fed an atherogenic diet. Longitudinal tracing of mineral formation in the aortic arch of these mice revealed the presence of mineral in vehicle- but not ML290-treated mice after 15 weeks of diet. Accelerated mineral growth was observed in vehicle-treated mice after 20 weeks of the diet, which was reduced by ML290 treatment. In humanized mice with CKD, ML290 significantly prevented ( P = 0.0344, n = 9) medial calcification. In vitro , ML290 reduced ( P = 0.0005, n = 3) superoxide production under osteogenic conditions in vascular smooth muscle cells (VSMCs). Osteogenic changes in VSMC phenotype associate with a release of alkaline phosphatase (ALP) in extracellular vesicles (EVs), which promote mineralization. ML290 treatment significantly ( P = 0.0001, n = 3) suppressed the formation of ALP-loaded EVs in vitro . Bone morphogenetic protein-4, an inducer of osteogenic transitions, and caveolin-1, a scaffolding protein required for calcifying EV formation, were significantly ( P = 0.0059, n = 4) down-regulated after 24 h treatment with ML290 compared to vehicle-treated VSMCs under osteogenic conditions. Conclusions: We demonstrate the therapeutic potential for ML290 to mitigate atherosclerosis and CKD-induced vascular calcification in vivo . The actions of ML290 to prevent medial calcification are in part attributed to its ability to limit the release of calcifying EVs as a result of osteogenic differentiation, and to reduce vascular superoxide production.

scholarly journals Cardiovascular Biomarkers in Chronic Kidney Disease

2010 ◽  
Vol 29 (4) ◽  
pp. 298-303 ◽  
Author(s):  
Mirjana Đerić ◽  
Velibor Čabarkapa
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Disease ◽  
Left Ventricular ◽  
Calcium Phosphorus ◽  
Traditional Risk Factors ◽  
Cardiovascular Biomarkers

Cardiovascular Biomarkers in Chronic Kidney DiseaseCardiovascular morbidity and mortality are markedly increased in chronic renal failure patients. Although it cannot be regarded as a cardiovascular disease risk equivalent, kidney dysfunction is considered an independent predictor of increased cardiovascular risk that increases with deteriorating kidney function. The association is a very complex one, and the term cardiorenal syndrome is now widely used. Cardiovascular disease in chronic kidney disease patients usually manifests as ischemic heart disease (in the form of angina, acute coronary syndrome or sudden cardiac death), cerebrovascular disease, peripheral vascular disease, and congestive heart failure. Vascular disease includes atherosclerosis and vascular calcifications, and cardiomyopathy comprises left ventricular hypertrophy, cardiac fibrosis and left ventricular systolic and diastolic dysfunction. In addition to the well-established traditional risk factors such as hypertension, hyperlipidemia, insulin resistance and diabetes mellitus, the association is supported by synergistic action of non-traditional risk factors such as excessive calcium-phosphorus load, hyperparathyroidism, anemia, hemodynamic overload, malnutrition, inflammation, hyperhomocysteinemia, altered nitric oxide synthase and increased oxidative stress. This paper summarizes the current understanding of the significance of specific uremic retention solutes, natriuretic peptides, biochemical markers of disorders in calcium-phosphorus homeostasis, systemic inflammation, oxidative stress, and dyslipidemia.

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