Association between plasma asymmetrical dimethylarginine activity and severity of aortic valve stenosis

Çağırcı, Göksel; Çay, Serkan; Çanğa, Aytun; Karakurt, Özlem; Yazıhan, Nuray; Kılıç, Harun; Topaloğlu, Serkan; Aras, Dursun; Demir, Ahmet Duran; Akdemir, Ramazan

doi:10.2459/jcm.0b013e32833cdcea

Cited by 17 publications

(11 citation statements)

References 31 publications

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“…Indeed, high serum levels of ADMA (≥0.779 µmol/L) predicted the presence of medial calcification in patients with CKD [145]. In addition, serum ADMA activity positively correlated with aortic valve stenosis severity in patients without CKD (serum ADMA activity: 1.94 ± 0.45 µmol/L in patients with severe aortic stenosis vs. 0.87 ± 0.37 µmol/L in patients with mild aortic stenosis ( p < 0.001)) [146]. In another study of patients with CKD, plasma ADMA levels were negatively correlated with the GFR and positively correlated with coronary artery calcification [147].…”

Section: The Impact Of Ckd On Macrophage Functions: Consequences Fmentioning

confidence: 99%

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

Hénaut¹,

Candellier

Boudot³

et al. 2019

Toxins

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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.

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Section: The Impact Of Ckd On Macrophage Functions: Consequences Fmentioning

confidence: 99%

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

Hénaut¹,

Candellier

Boudot³

et al. 2019

Toxins

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“…4,7,33,42,55,56 The progression of atherosclerosis results in a structural and cellular remodeling of the vasculature. 4,7,41,57 Changes that alter mineral metabolism, modify calcification regulators, or modulate vascular cell phenotype can have catastrophic consequences in vascular structures. 40,55,[58][59][60] Advanced calcific lesions can develop woven bone and even commence hematopoiesis.…”

Section: Vascular Calcificationmentioning

confidence: 99%

Atherosclerotic Calcification: Wnt Is the Hint

Albanese

Khan

Barratt

et al. 2018

JAHA

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“…First, endogenous inhibitors of nitric oxide synthase—such as asymmetric dimethylarginine—are significantly increased in patients with CAVS 87, 88 . Second, addition of exogenous NO slows calcium nodule formation in valve interstitial cells in vitro 51 .…”

Section: Endogenous Mechanisms That May Modulate Pro-calcific Signalimentioning

confidence: 99%

“…Nevertheless, targeting antioxidants to different subcellular compartments may be more beneficial than those which affect redox state throughout the cell 205 . Reducing oxidative stress is also likely to increase nitric oxide bioavailability 8, 68 , which may be augmented by combining antioxidant therapy with treatments that reduce endogenous inhibitors of nitric oxide synthases (i.e., asymmetric dimethylarginine, which is increased in patients with CAVS 87, 88 ).…”

Section: Interventions That May Inhibit Development And/or Progressiomentioning

confidence: 99%

Calcific Aortic Valve Stenosis: Methods, Models, and Mechanisms

Miller

Weiß

Heistad

2011

Circulation Research

277

218

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Calcific aortic valve stenosis (CAVS) is a major health problem facing aging societies. The identification of osteoblast-like and osteoclast-like cells in human tissue has led to a major paradigm shift in the field. CAVS was thought to be a passive, degenerative process, whereas now the progression of calcification in CAVS is considered to be actively regulated. Mechanistic studies examining the contributions of true ectopic osteogenesis, non-osseous calcification, and ectopic osteoblast-like cells (that appear to function differently from skeletal osteoblasts) to valvular dysfunction have been facilitated by the development of mouse models of CAVS. Recent studies also suggest that valvular fibrosis, as well as calcification, may play an important role in restricting cusp movement, and CAVS may be more appropriately viewed as a fibrocalcific disease. High resolution echocardiography and magnetic resonance imaging have emerged as useful tools for testing the efficacy of pharmacological and genetic interventions in vivo. Key studies in humans and animals are reviewed that have shaped current paradigms in the field of CAVS, and suggest promising future areas for research.

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Association between plasma asymmetrical dimethylarginine activity and severity of aortic valve stenosis

Cited by 17 publications

References 31 publications

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

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

Atherosclerotic Calcification: Wnt Is the Hint

Calcific Aortic Valve Stenosis: Methods, Models, and Mechanisms

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