&lt;p&gt;Vascular Calcification: An Important Understanding in Nephrology&lt;/p&gt;

Vahed, Sepideh Zununi; Mostafavi, Soroush; Khatibi, Seyed Mahdi Hosseiniyan; Shoja, Mohammadali Mohajel; Ardalan, Mohammadreza

doi:10.2147/vhrm.s242685

Cited by 41 publications

(25 citation statements)

References 133 publications

(132 reference statements)

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“…Excess phosphorus and calcium molecules deposit can further drive VSMCs undergo osteogenesis. This phenotypic switch induces a variety of behavioral changes as trans-differentiated VSMCs adopt the characteristics of synthetic cells that include high elastase secretion, aberrant senescence, migration, apoptosis and induction of extracellular pro-calcifying vesicles release that promote the formation of hydroxyapatite crystals, thus promoting local calcification [ 33 , 34 , 35 ]. The pro-calcifying vesicles released by VSMCs are of two types: matrix vesicles (30–300 nm in diameter) and apoptotic bodies (50–5000 nm in diameter) [ 36 ].…”

Section: Uremic Toxin Mediated Pathways Leading To Vascular Calcifmentioning

confidence: 99%

Role of Uremic Toxins in Early Vascular Ageing and Calcification

Kyriakidis

Cobo²,

Dai

et al. 2021

Toxins

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In patients with advanced chronic kidney disease (CKD), the accumulation of uremic toxins, caused by a combination of decreased excretion secondary to reduced kidney function and increased generation secondary to aberrant expression of metabolite genes, interferes with different biological functions of cells and organs, contributing to a state of chronic inflammation and other adverse biologic effects that may cause tissue damage. Several uremic toxins have been implicated in severe vascular smooth muscle cells (VSMCs) changes and other alterations leading to vascular calcification (VC) and early vascular ageing (EVA). The above mentioned are predominant clinical features of patients with CKD, contributing to their exceptionally high cardiovascular mortality. Herein, we present an update on pathophysiological processes and mediators underlying VC and EVA induced by uremic toxins. Moreover, we discuss their clinical impact, and possible therapeutic targets aiming at preventing or ameliorating the harmful effects of uremic toxins on the vasculature.

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Section: Uremic Toxin Mediated Pathways Leading To Vascular Calcifmentioning

confidence: 99%

Role of Uremic Toxins in Early Vascular Ageing and Calcification

Kyriakidis

Cobo²,

Dai

et al. 2021

Toxins

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“…VC is an active biological process associated with hydroxyapatite crystallisation in the vascular wall. The decline of inhibitors such as Matrix Gla Protein (MGP), Gla‐rich protein (GRP), osteoprotegerin (OPG), bone morphogenetic protein 7 (BMP‐7) and the increase of calcification inducers lead to more extensive VC in the CKD population 13,14 . Furthermore, uremic toxins, calcium and phosphate metabolism dysfunction may directly influence VSMCs' physiological function, leading to irregular senescence, proliferation and migration of VSMC, ultimately leading to VC.…”

Section: Vc In Ckdmentioning

confidence: 99%

Role of gut microbiota‐derived metabolites on vascular calcification in CKD

Yin

Ghosh

et al. 2020

J Cellular Molecular Medi

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The interaction between gut microbiota and the host has gained widespread concern. Gut microbiota not only provides nutrients from the ingested food but also generates bioactive metabolites and signalling molecules to impact host physiology, especially in chronic kidney disease (CKD). The development of CKD, accompanied by changed diet and medication, alters the gut flora and causes the effect in distant organs, leading to clinical complications. Vascular calcification (VC) is an actively regulated process and a high prevalence of VC in CKD has also been linked to an imbalance in gut microbiota and altered metabolites. In this review, we focused on gut microbiota‐derived metabolites involved in VC in CKD and explained how these metabolites influence the calcification process. Correcting the imbalance of gut microbiota and regulating microbiota‐derived metabolites by dietary modification and probiotics are new targets for the improvement of the gut‐kidney axis, which indicate innovative treatment options of VC in CKD.

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“…It is now well established that several different mechanisms (such as inflammation and oxidative stress) enhance VC in CKD patients [10]. Moreover, the high prevalence of VC in CKD is associated with the accumulation of uremic toxins that can have a major impact on vascular remodeling [11].…”

Section: Classification Of Evsmentioning

confidence: 99%

“…This dysregulation prompts vascular smooth muscle cells (VSMCs) found in the media layer of blood vessels to turn into osteoblast-like cells; this switching may have an important role in the onset of VC [ 9 ]. However, other cells (such as osteoclast-like cells, endothelial progenitor cells and Gli1+ mesenchymal stem cells (MSCs)) are also involved in VC [ 10 ]. It is now well established that several different mechanisms (such as inflammation and oxidative stress) enhance VC in CKD patients [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

“…However, other cells (such as osteoclast-like cells, endothelial progenitor cells and Gli1+ mesenchymal stem cells (MSCs)) are also involved in VC [ 10 ]. It is now well established that several different mechanisms (such as inflammation and oxidative stress) enhance VC in CKD patients [ 10 ]. Moreover, the high prevalence of VC in CKD is associated with the accumulation of uremic toxins that can have a major impact on vascular remodeling [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of Chronic Kidney Disease and Uremic Toxins on Extracellular Vesicle Biology

Yaker

Kamel

Ausseil

et al. 2020

Toxins

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Vascular calcification (VC) is a cardiovascular complication associated with a high mortality rate, especially in patients with diabetes, atherosclerosis or chronic kidney disease (CKD). In CKD patients, VC is associated with the accumulation of uremic toxins, such as indoxyl sulphate or inorganic phosphate, which can have a major impact in vascular remodeling. During VC, vascular smooth muscle cells (VSMCs) undergo an osteogenic switch and secrete extracellular vesicles (EVs) that are heterogeneous in terms of their origin and composition. Under physiological conditions, EVs are involved in cell-cell communication and the maintenance of cellular homeostasis. They contain high levels of calcification inhibitors, such as fetuin-A and matrix Gla protein. Under pathological conditions (and particularly in the presence of uremic toxins), the secreted EVs acquire a pro-calcifying profile and thereby act as nucleating foci for the crystallization of hydroxyapatite and the propagation of calcification. Here, we review the most recent findings on the EVs’ pathophysiological role in VC, the impact of uremic toxins on EV biogenesis and functions, the use of EVs as diagnostic biomarkers and the EVs’ therapeutic potential in CKD.

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<p>Vascular Calcification: An Important Understanding in Nephrology</p>

Cited by 41 publications

References 133 publications

Role of Uremic Toxins in Early Vascular Ageing and Calcification

Role of Uremic Toxins in Early Vascular Ageing and Calcification

Role of gut microbiota‐derived metabolites on vascular calcification in CKD

Effects of Chronic Kidney Disease and Uremic Toxins on Extracellular Vesicle Biology

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