An update on vascular calcification and potential therapeutics

Singh, Anubha; Tandon, Simran; Tandon, Chanderdeep

doi:10.1007/s11033-020-06086-y

Cited by 56 publications

(53 citation statements)

References 91 publications

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“…Current treatment options for AMC focus on slowing the progression of arterial calcification and attempt to attenuate common risk factors such as hyperphosphatemia and hypercalcemia. These treatments, including phosphate binders, calcimimetics, and control of active vitamin D levels, lack efficacy since they target risk factors but do not directly inhibit calcification [9]. Therefore, effective therapeutic strategies directly blocking the development and/or progression of the calcification process are necessary.…”

Section: Introductionmentioning

confidence: 99%

Endothelial Contribution to Warfarin-Induced Arterial Media Calcification in Mice

Bergh

Moudt

Branden

et al. 2021

IJMS

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Arterial media calcification (AMC) is predominantly regulated by vascular smooth muscle cells (VSMCs), which transdifferentiate into pro-calcifying cells. In contrast, there is little evidence for endothelial cells playing a role in the disease. The current study investigates cellular functioning and molecular pathways underlying AMC, respectively by, an ex vivo isometric organ bath set-up to explore the interaction between VSMCs and ECs and quantitative proteomics followed by functional pathway interpretation. AMC development, which was induced in mice by dietary warfarin administration, was proved by positive Von Kossa staining and a significantly increased calcium content in the aorta compared to that of control mice. The ex vivo organ bath set-up showed calcified aortic segments to be significantly more sensitive to phenylephrine induced contraction, compared to control segments. This, together with the fact that calcified segments as compared to control segments, showed a significantly smaller contraction in the absence of extracellular calcium, argues for a reduced basal NO production in the calcified segments. Moreover, proteomic data revealed a reduced eNOS activation to be part of the vascular calcification process. In summary, this study identifies a poor endothelial function, next to classic pro-calcifying stimuli, as a possible initiator of arterial calcification.

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Section: Introductionmentioning

confidence: 99%

Endothelial Contribution to Warfarin-Induced Arterial Media Calcification in Mice

Bergh

Moudt

Branden

et al. 2021

IJMS

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“…The pathophysiological mechanisms leading to vascular calcification are still unclear, therefore, at present, there is no comprehensive treatment to prevent or counteract it. The current strategies are based on the modulation of its key regulators, such as vitamin D, calcium, phosphate, through calcimimetics, vitamin D analogs, and phosphate binders [ 21 , 25 ]. Phosphate binders limit dietary phosphate absorption, lowering its serum levels, and are used in clinical practice to manage hyperphosphatemia in CKD patients.…”

Section: Pharmacological Approaches For the Treatment Of Vascular Calcificationmentioning

confidence: 99%

The Emerging Role of Nutraceuticals in Cardiovascular Calcification: Evidence from Preclinical and Clinical Studies

et al. 2021

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Cardiovascular calcification is the ectopic deposition of calcium-phosphate crystals within the arterial wall and the aortic valve leaflets. This pathological process leads to increased vascular stiffness, reduced arterial elasticity, and aortic valve stenosis, increasing the risk of cardiovascular diseases. Although cardiovascular calcification is an increasing health care burden, to date no medical therapies have been approved for treating or preventing it. Considering the current lack of therapeutic strategies and the increasing prevalence of cardiovascular calcification, the investigation of some nutraceuticals to prevent this pathological condition has become prevalent in recent years. Recent preclinical and clinical studies evaluated the potential anti-calcific role of nutraceuticals (including magnesium, zinc, iron, vitamin K, and phytate) in the progression of vascular calcification, providing evidence for their dietary supplementation, especially in high-risk populations. The present review summarizes the current knowledge and latest advances for nutraceuticals with the most relevant preclinical and clinical data, including magnesium, zinc, iron, vitamin K, and phytate. Their supplementation might be recommended as a cost-effective strategy to avoid nutritional deficiency and to prevent or treat cardiovascular calcification. However, the optimal dose of nutraceuticals has not been identified and large interventional trials are warranted to support their protective effects on cardiovascular disease.

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“…However, no efficient therapy is approved for the treatment of VC until now, although various treatment strategies targeting pathological conditions (CKD, cardiovascular disease and osteoporosis) are available. These interventions include phosphate binders, sodium thiosulphate, calcimimetics, vitamin K, vitamin D, myoinositol, denosumab, and tissue-nonspecific alkaline phosphatase inhibitors (Singh et al, 2021). Several studies to date have demonstrated that the overexpression or inhibition of non-coding RNAs (ncRNAs) may provide promising avenues for VC therapy.…”

Section: Introductionmentioning

confidence: 99%

Bibliometric and Visual Analysis of Vascular Calcification Research

et al. 2021

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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.

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An update on vascular calcification and potential therapeutics

Cited by 56 publications

References 91 publications

Endothelial Contribution to Warfarin-Induced Arterial Media Calcification in Mice

Endothelial Contribution to Warfarin-Induced Arterial Media Calcification in Mice

The Emerging Role of Nutraceuticals in Cardiovascular Calcification: Evidence from Preclinical and Clinical Studies

Bibliometric and Visual Analysis of Vascular Calcification Research

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