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Journal articles on the topic 'Arterial calcification'

Author: Grafiati

Published: 4 June 2021

Last updated: 3 February 2022

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1

Bartstra, Jonas W., Wilko Spiering, Jody M. W. van den Ouweland, Willem P. T. M. Mali, Rob Janssen, and Pim A. de Jong. "Increased Elastin Degradation in Pseudoxanthoma Elasticum Is Associated with Peripheral Arterial Disease Independent of Calcification." Journal of Clinical Medicine 9, no. 9 (2020): 2771. http://dx.doi.org/10.3390/jcm9092771.

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Pseudoxanthoma elasticum (PXE) results in extensive fragmentation and calcification of elastin fibers in the peripheral arteries, which results in peripheral arterial disease (PAD). Current research focuses on the role of calcifications in the pathogenesis of PXE. Elastin degradation and calcification are shown to interact and may amplify each other. This study aims to compare plasma desmosines, a measure of elastin degradation, between PXE patients and controls and to investigate the association between desmosines and (1) arterial calcification, (2) PAD, and (3) PAD independent of arterial ca

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2

Schurgers, Leon J., Hermann Aebert, Cees Vermeer, Burkhard Bültmann, and Jan Janzen. "Oral anticoagulant treatment: friend or foe in cardiovascular disease?" Blood 104, no. 10 (2004): 3231–32. http://dx.doi.org/10.1182/blood-2004-04-1277.

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Abstract Calcification is a common complication in cardiovascular disease and may affect both arteries and heart valves. Matrix γ-carboxyglutamic acid (Gla) protein (MGP) is a potent inhibitor of vascular calcification, the activity of which is regulated by vitamin K. In animal models, vitamin K antagonists (oral anticoagulants [OACs]) were shown to induce arterial calcification. To investigate whether long-term OAC treatment may induce calcification in humans also, we have measured the grade of aortic valve calcification in patients with and without preoperative OAC treatment. OAC-treated sub

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3

Kei, Olivia C. Y., Walter J. Duncan, and Derek G. Human. "Pulmonary arterial and intracranial calcification in the recipient of a twin–twin transfusion." Cardiology in the Young 12, no. 5 (2002): 488–90. http://dx.doi.org/10.1017/s1047951102000859.

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Pulmonary arterial and intracranial calcifications are rarely found in children. A female infant, the recipient of a twin–twin transfusion syndrome was found, by ultrasound and computed tomography, to have both pulmonary arterial and intracerebral calcification. A rare condition, termed idiopathic arterial calcification of infancy, is the likely cause. This condition carries a poor prognosis and is usually fatal.

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4

Devriese, Magali, Anne Legrand, Marie-Cécile Courtois, Xavier Jeunemaitre, and Juliette Albuisson. "Pseudoxanthoma elasticum with prominent arterial calcifications evoking CD73 deficiency." Vascular Medicine 24, no. 5 (2019): 461–64. http://dx.doi.org/10.1177/1358863x19853360.

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Pseudoxanthoma elasticum (PXE) is a rare disorder characterized by skin, eye, and cardiovascular lesions due to ectopic mineralization and fragmentation of elastic fibers of connective tissues. We present an atypical case of PXE with diffuse vascular calcification and negligible skin and eye lesions. The patient was a 37-year-old man suffering from severe bilateral arterial calcifications in superficial femoral and posterior tibial arteries. Eye fundoscopy and skin examination were first considered normal. This phenotype suggested first the diagnosis of Arterial Calcification due to Deficiency

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5

Seely, Stephen. "On arterial calcification." International Journal of Cardiology 61, no. 2 (1997): 105–8. http://dx.doi.org/10.1016/s0167-5273(97)00131-9.

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6

Ho, Chin Yee, and Catherine M. Shanahan. "Medial Arterial Calcification." Arteriosclerosis, Thrombosis, and Vascular Biology 36, no. 8 (2016): 1475–82. http://dx.doi.org/10.1161/atvbaha.116.306717.

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7

Polonsky, Tamar S., and Philip Greenland. "Breast Arterial Calcification." Circulation 135, no. 6 (2017): 499–501. http://dx.doi.org/10.1161/circulationaha.116.025277.

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8

Lanzer, Peter, Fadil M. Hannan, Jan D. Lanzer, et al. "Medial Arterial Calcification." Journal of the American College of Cardiology 78, no. 11 (2021): 1145–65. http://dx.doi.org/10.1016/j.jacc.2021.06.049.

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9

Bäck, Magnus, and Jean-Baptiste Michel. "From organic and inorganic phosphates to valvular and vascular calcifications." Cardiovascular Research 117, no. 9 (2021): 2016–29. http://dx.doi.org/10.1093/cvr/cvab038.

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Abstract Calcification of the arterial wall and valves is an important part of the pathophysiological process of peripheral and coronary atherosclerosis, aortic stenosis, ageing, diabetes, and chronic kidney disease. This review aims to better understand how extracellular phosphates and their ability to be retained as calcium phosphates on the extracellular matrix initiate the mineralization process of arteries and valves. In this context, the physiological process of bone mineralization remains a human model for pathological soft tissue mineralization. Soluble (ionized) calcium precipitation

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10

Rennenberg, Roger J. M. W., Bernard J. van Varik, Leon J. Schurgers, et al. "Chronic coumarin treatment is associated with increased extracoronary arterial calcification in humans." Blood 115, no. 24 (2010): 5121–23. http://dx.doi.org/10.1182/blood-2010-01-264598.

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Abstract Vascular calcification is a marker of increased cardiovascular risk. Vitamin K–dependent matrix Gla protein (MGP) is important in inhibiting calcification. Because MGP activation is vitamin K dependent, we performed a cross-sectional study investigating the relationship between the use of vitamin K antagonists and extracoronary vascular calcification. From the Dutch thrombosis services we selected 19 patients younger than 55 years who had no other cardiovascular risk factors and who had used coumarins for more than 10 years, and compared these to 18 matched healthy controls. MGP was m

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11

Stavrinou, Eirini, Aikaterini Papagianni, Charalambos Koumaras, Panagiotis Pateinakis, and Georgios Efstratiadis. "Can We Tackle with Vascular Calcification and Arterial Stiffness in Patients with Chronic Kidney Disease?" Open Hypertension Journal 5, no. 1 (2013): 63–66. http://dx.doi.org/10.2174/1876526201305010063.

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Cardiovascular disease remains the leading cause of increased morbidity and mortality in patients with chronic kidney disease and is attributed to early and accelerated atherosclerosis and arteriosclerosis observed in this patient population. Vascular calcifications, particularly of the media, are commonly found in chronic uremia and are a major contributor to arteriosclerosis and increased arterial stiffness. Epidemiologic data support the correlation of vascular calcification and arterial stiffness to adverse cardiovascular outcomes and mortality. Experimental evidence has shed light on the

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12

Jha, Anamika, Anugya Sah, Birendra Raj Joshi, and Benu Lohani. "Breast Arterial Calcifications on Mammography among Patients Attending the Radiology Department in a Tertiary Care Centre: A Descriptive Cross-sectional Study." Journal of Nepal Medical Association 59, no. 241 (2021): 844–47. http://dx.doi.org/10.31729/jnma.6922.

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Introduction: Breast arterial calcifications are common mammographic findings which are associated with coronary artery disease. The aim of this study was to find the prevalence of breast arterial calcifications in women presenting for mammography in a tertiary care centre. Methods: This descriptive cross-sectional study was performed in the Department of Radiology, in a tertiary care hospital after taking ethical clearance, Reference number 352(6-11)E-2, 077/078, data was collected from Syngovia database from March-June 2021 which included 1614 mammograms. Convenience sampling was done and ma

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13

Olesen, Ping, Kirsten Nguyen, Lise Wogensen, Thomas Ledet, and Lars Melholt Rasmussen. "Calcification of human vascular smooth muscle cells: associations with osteoprotegerin expression and acceleration by high-dose insulin." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 2 (2007): H1058—H1064. http://dx.doi.org/10.1152/ajpheart.00047.2006.

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Arterial medial calcifications occur often in diabetic individuals as part of the diabetic macroangiopathy. The pathogenesis is unknown, but the presence of calcifications predicts risk of cardiovascular events. We examined the effects of insulin on calcifying smooth muscle cells in vitro and measured the expression of the bone-related molecule osteoprotegerin (OPG). Human vascular smooth muscle cells (VSMCs) were grown from aorta from kidney donors. Induction of calcification was performed with β-glycerophosphate. The influence of insulin (200 μU/ml or 1,000 μU/ml) on calcification was judged

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14

Nicoll, Rachel. "Correlation between coronary and valve calcification: Review of current evidence." International Cardiovascular Forum Journal 1, no. 1 (2015): 19. http://dx.doi.org/10.17987/icfj.v1i1.10.

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<p>We carried out a review of the correlation between calcification of different arteries and valves and their risk factors to determine the extent of the association. We found a strong correlation between calcification presence, extent and progression between different arterial beds and the aortic valve, suggesting that calcification is a systemic diffuse disease, affecting the arterial tree as a whole. Despite this strong association, a comparison between coronary artery calcification (CAC) and calcification of other arteries may not be strictly valid, since only intimal calcification

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15

Wen, Ke-xin, Mohammad Arfan Ikram, Oscar H. Franco, et al. "Association of migraine with calcification in major vessel beds: The Rotterdam Study." Cephalalgia 39, no. 8 (2019): 1041–48. http://dx.doi.org/10.1177/0333102419843148.

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Background To explore the role of large-artery atherosclerosis in migraine, we investigated the association between migraine and arterial calcification in different intracranial and extracranial vessels. Methods 1856 participants were included, mean age (standard deviation) 67.4 (5.8) years, from the population-based Rotterdam Study cohort. Migraine was assessed by validated questionnaire and vascular calcification was assessed by computed tomography (expressed in Agatston score for the coronary arteries and volume in mm3 for the aortic arch, intracranial, and extracranial carotid arteries). P

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16

Konijn, Louise C. D., Richard A. P. Takx, Willem P. Th M. Mali, Hugo T. C. Veger, and Hendrik van Overhagen. "Different Lower Extremity Arterial Calcification Patterns in Patients with Chronic Limb-Threatening Ischemia Compared with Asymptomatic Controls." Journal of Personalized Medicine 11, no. 6 (2021): 493. http://dx.doi.org/10.3390/jpm11060493.

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Objectives: The most severe type of peripheral arterial disease (PAD) is critical limb-threatening ischemia (CLI). In CLI, calcification of the vessel wall plays an important role in symptoms, amputation rate, and mortality. However, calcified arteries are also found in asymptomatic persons (non-PAD patients). We investigated whether the calcification pattern in CLI patients and non- PAD patients are different and could possibly explain the symptoms in CLI patients. Materials and Methods: 130 CLI and 204 non-PAD patients underwent a CT of the lower extremities. This resulted in 118 CLI patient

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17

Adragao, Teresa, Patrícia Branco, Rita Birne, et al. "Bone Mineral Density, Vascular Calcifications, and Arterial Stiffness in Peritoneal Dialysis Patients." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 28, no. 6 (2008): 668–72. http://dx.doi.org/10.1177/089686080802800621.

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The objective of this study was to evaluate the correlation of bone mineral density (BMD), evaluated by DXA, with vascular calcifications, arterial stiffness, and vascular disease in patients on peritoneal dialysis. Vascular calcifications were evaluated by vascular calcification score on plain x ray, and arterial stiffness was measured by pulse wave velocity using the Complior device (Artech Medical, Pantin, France). Adjusting for multiple factors, lower BMD at the femoral neck, but not at the lumbar spine, was associated with higher pulse wave velocity ( p = 0.037), higher vascular calcifica

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18

Watchmaker, Lauren E., Jennifer M. Watchmaker, and Greg P. Watchmaker. "Arterial Calcification on Wrist Radiographs May Suggest Need for Evaluation of Atherosclerosis in Asymptomatic Individuals." Case Reports in Radiology 2019 (July 3, 2019): 1–3. http://dx.doi.org/10.1155/2019/6156948.

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Asymptomatic individuals with significant coronary artery disease (CAD) are at risk for unanticipated cardiac events including myocardial infarction (MI). Laboratory studies, stress tests, and coronary artery imaging including coronary artery calcium (CAC) scoring evaluate at-risk individuals. Hand and wrist x-rays demonstrating significant arterial wall calcification may provide an additional means to identify asymptomatic individuals at risk for cardiac events. Here we report a case series of patients without known cardiac disease who demonstrated significant calcium deposits in the radial a

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19

Irvine, G. B., and R. N. W. Chan. "ARTERIAL CALCIFICATION AND TOURNIQUETS." Lancet 328, no. 8517 (1986): 1217. http://dx.doi.org/10.1016/s0140-6736(86)92221-x.

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20

Fish, Richard S., Enriko Klootwijk, Frederick W. K. Tam, et al. "ATP and arterial calcification." European Journal of Clinical Investigation 43, no. 4 (2013): 405–12. http://dx.doi.org/10.1111/eci.12055.

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21

Rutsch, Frank, Yvonne Nitschke, and Robert Terkeltaub. "Genetics in Arterial Calcification." Circulation Research 109, no. 5 (2011): 578–92. http://dx.doi.org/10.1161/circresaha.111.247965.

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22

Li, Jonathan Z., and William Huen. "Calciphylaxis with Arterial Calcification." New England Journal of Medicine 357, no. 13 (2007): 1326. http://dx.doi.org/10.1056/nejmicm060859.

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23

Proesmans, Willem, and Maria Van Dyck. "Idiopathic infantile arterial calcification." Pediatric Nephrology 5, no. 1 (1991): 96. http://dx.doi.org/10.1007/bf00852858.

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24

Chen, Neal X., and Sharon M. Moe. "Arterial calcification in diabetes." Current Diabetes Reports 3, no. 1 (2003): 28–32. http://dx.doi.org/10.1007/s11892-003-0049-2.

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25

Fuchs, U., P. Caffier, H. G. Schulz, and P. Wieniecki. "Arterial calcification in diabetics." Virchows Archiv A Pathological Anatomy and Histopathology 407, no. 4 (1985): 431–39. http://dx.doi.org/10.1007/bf00709989.

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26

Taylor, Charlotte, Lukasz P. Zielinski, Mohammed M. Chowdhury, and Patrick A. Coughlin. "Defining the Role of Duplex Ultrasound Assessment to Determine Severity of Arterial Calcification: An Analysis of the Superficial Femoral Artery." Journal for Vascular Ultrasound 44, no. 2 (2020): 74–78. http://dx.doi.org/10.1177/1544316720910550.

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Lower limb arterial calcification associates with poor cardiovascular outcomes. The gold standard method of assessment is via computed tomography, yet duplex is our primary imaging modality. Currently, there is no standardized objective assessment of lower limb arterial calcification using duplex. We aimed to define the role of duplex in the assessment of lower limb arterial calcification. Initial consensus was achieved between a cohort of vascular scientists on objective imaging specific markers of lower limb arterial calcification severity using duplex. This resulted in objective description

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27

Janzen, Katrin, and Jan Janzen. "Arterial Microcalcifications in the Breast Mimicking Malignancy." Case Reports in Radiology 2012 (2012): 1–2. http://dx.doi.org/10.1155/2012/946317.

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Microcalcifications in the breast are highly suggestive of malignancy; they can occur in many pathological conditions. A 36-years-old nondiabetic woman came to the gynaecologist with a suspect palpable mass in the upper outer quadrant of the right breast. Histopathological examination confirmed a calcification of a small artery (diameter: 0.45 mm). Arterial calcifications can mimic a malignant lesion in the breast.

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28

Luo, Xiang-Hang, Li-Ling Zhao, Ling-Qing Yuan, Min Wang, Hui Xie, and Er-Yuan Liao. "Development of Arterial Calcification in Adiponectin-Deficient Mice: Adiponectin Regulates Arterial Calcification." Journal of Bone and Mineral Research 24, no. 8 (2009): 1461–68. http://dx.doi.org/10.1359/jbmr.090227.

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29

Oh, Lawrence Chia-Wei, Kenneth Kwok-Pan Lau, Ashwini Devapalasundaram, Kevin Buchan, Ahilan Kuganesan, and Minh Huynh. "Efficacy of fine focal spot technique in CT angiography of neck." British Journal of Radiology 92, no. 1100 (2019): 20190083. http://dx.doi.org/10.1259/bjr.20190083.

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Objectives: Focal spot size partially defines spatial resolution of a CT system. Many CT tubes have two focal spot sizes, with the finer one allowing more detailed imaging at the cost of photon intensity and increased heat production. Improved X-ray technology and advancement of various generations of iterative reconstruction allow the use of fine focal spot technique in CT angiography. CT neck angiography (CTNA) has been commonly performed as part of stroke imaging or in the trauma setting. This prospective study aimed to assess the efficacy of fine focal spot scanning in vessel clarity impro

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30

Bishop, Paul D., Lindsay E. Feiten, Kenneth Ouriel, et al. "Arterial Calcification Increases in Distal Arteries in Patients with Peripheral Arterial Disease." Annals of Vascular Surgery 22, no. 6 (2008): 799–805. http://dx.doi.org/10.1016/j.avsg.2008.04.008.

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31

Saito, Yukihiro, Kazufumi Nakamura, and Hiroshi Ito. "Effects of Eicosapentaenoic Acid on Arterial Calcification." International Journal of Molecular Sciences 21, no. 15 (2020): 5455. http://dx.doi.org/10.3390/ijms21155455.

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Arterial calcification is a hallmark of advanced atherosclerosis and predicts cardiovascular events. However, there is no clinically accepted therapy that prevents progression of arterial calcification. HMG-CoA reductase inhibitors, statins, lower low-density lipoprotein-cholesterol and reduce cardiovascular events, but coronary artery calcification is actually promoted by statins. The addition of eicosapentaenoic acid (EPA) to statins further reduced cardiovascular events in clinical trials, JELIS and REDUCE-IT. Additionally, we found that EPA significantly suppressed arterial calcification i

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32

Ekim, Mesiha, Suat Fitoz, Z. Birsin Ozcakar, and Fatos Yalcinkaya. "Vascular Calcification in an Adolescent Treated with Long-Term Peritoneal Dialysis." International Journal of Nephrology 2011 (2011): 1–4. http://dx.doi.org/10.4061/2011/702406.

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The reason of high mortality in patients with chronic kidney disease (CKD) is cardiovascular disease and arterial calcification has been accepted as an additive factor on this status. In this report we described vascular and cardiac valvular calcifications in an adolescent on CAPD.

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33

Opdebeeck, Britt, Patrick C. D’Haese, and Anja Verhulst. "Molecular and Cellular Mechanisms that Induce Arterial Calcification by Indoxyl Sulfate and P-Cresyl Sulfate." Toxins 12, no. 1 (2020): 58. http://dx.doi.org/10.3390/toxins12010058.

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The protein-bound uremic toxins, indoxyl sulfate (IS) and p-cresyl sulfate (PCS), are considered to be harmful vascular toxins. Arterial media calcification, or the deposition of calcium phosphate crystals in the arteries, contributes significantly to cardiovascular complications, including left ventricular hypertrophy, hypertension, and impaired coronary perfusion in the elderly and patients with chronic kidney disease (CKD) and diabetes. Recently, we reported that both IS and PCS trigger moderate to severe calcification in the aorta and peripheral vessels of CKD rats. This review describes t

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34

Knisely, A. S. "Idiopathic Arterial calcification of infancy." Human Pathology 17, no. 5 (1986): 534. http://dx.doi.org/10.1016/s0046-8177(86)80047-8.

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35

Karthikeyan, Gengaimuthu. "Generalized Arterial Calcification of Infancy." Journal of Pediatrics 162, no. 5 (2013): 1074–1074. http://dx.doi.org/10.1016/j.jpeds.2012.11.015.

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36

Stabley, John N., and Dwight A. Towler. "Arterial Calcification in Diabetes Mellitus." Arteriosclerosis, Thrombosis, and Vascular Biology 37, no. 2 (2017): 205–17. http://dx.doi.org/10.1161/atvbaha.116.306258.

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37

Sutton, Nadia R., and Marion A. Hofmann Bowman. "Reining in Peripheral Arterial Calcification." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 7 (2020): 1614–16. http://dx.doi.org/10.1161/atvbaha.120.314665.

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38

Arroyo, L. G., M. A. Hayes, J. DeLay, C. Rao, B. Duncan, and L. Viel. "Arterial Calcification in Race Horses." Veterinary Pathology 45, no. 5 (2008): 617–25. http://dx.doi.org/10.1354/vp.45-5-617.

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39

Epstein, Murray, and Henry R. Black. "Arterial Calcification and Calcium Antagonists." Hypertension 37, no. 6 (2001): 1414–15. http://dx.doi.org/10.1161/01.hyp.37.6.1414.

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40

Donuru, Achala, Vinay Kandula, Edward Oliver, and David Saul. "Generalized Arterial Calcification of Infancy." Radiology: Cardiothoracic Imaging 2, no. 4 (2020): e190226. http://dx.doi.org/10.1148/ryct.2020190226.

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41

Qadri, Syed Irfan, and Abhilash Koratala. "Calciphylaxis with extensive arterial calcification." Clinical Case Reports 5, no. 8 (2017): 1418–19. http://dx.doi.org/10.1002/ccr3.1068.

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42

Van Reempts, P. J., K. J. Boven, S. E. Spitaels, A. M. Roodhooft, E. L. J. Vercruyssen, and K. J. Van Acker. "Idiopathic arterial calcification of infancy." Calcified Tissue International 48, no. 1 (1991): 1–6. http://dx.doi.org/10.1007/bf02555789.

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43

Nicoll, Rachel, and Michael Y. Henein. "Arterial calcification: Friend or foe?" International Journal of Cardiology 167, no. 2 (2013): 322–27. http://dx.doi.org/10.1016/j.ijcard.2012.06.110.

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44

Yazisiz, Veli, Ali Berkant Avci, and Ender Terzioğlu. "Arterial calcification in rheumatoid arthritis." Artery Research 2, no. 1 (2008): 49. http://dx.doi.org/10.1016/j.artres.2007.10.001.

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45

Proudfoot, Diane. "Molecular mechanisms of arterial calcification." Artery Research 3, no. 4 (2009): 128. http://dx.doi.org/10.1016/j.artres.2009.10.001.

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46

Nicoll, R., and M. Henein. "Arterial calcification: A new perspective?" International Journal of Cardiology 228 (February 2017): 11–22. http://dx.doi.org/10.1016/j.ijcard.2016.11.099.

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47

Wu, Shan-Shan, Xiao Lin, Ling-Qing Yuan, and Er-Yuan Liao. "The Role of Epigenetics in Arterial Calcification." BioMed Research International 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/320849.

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Arterial calcification is highly prevalent and correlated with cardiovascular mortality, especially in patients with ESRD or diabetes. The pathogenesis of arterial calcification is multifactorial, with both genetic and environmental factors being implicated. In recent years, several mechanisms contributing to arterial calcification have been proposed. However, these can only explain a small proportion of the variability in arterial calcification, which is a major obstacle for its prevention and management. Epigenetics has emerged as one of the most promising areas that may fill in some of the

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48

Min, Hosung, Sean Morony, Ildiko Sarosi, et al. "Osteoprotegerin Reverses Osteoporosis by Inhibiting Endosteal Osteoclasts and Prevents Vascular Calcification by Blocking a Process Resembling Osteoclastogenesis." Journal of Experimental Medicine 192, no. 4 (2000): 463–74. http://dx.doi.org/10.1084/jem.192.4.463.

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High systemic levels of osteoprotegerin (OPG) in OPG transgenic mice cause osteopetrosis with normal tooth eruption and bone elongation and inhibit the development and activity of endosteal, but not periosteal, osteoclasts. We demonstrate that both intravenous injection of recombinant OPG protein and transgenic overexpression of OPG in OPG−/2 mice effectively rescue the osteoporotic bone phenotype observed in OPG-deficient mice. However, intravenous injection of recombinant OPG over a 4-wk period could not reverse the arterial calcification observed in OPG−/− mice. In contrast, transgenic OPG

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49

Opdebeeck, Britt, Isabel R. Orriss, Ellen Neven, Patrick C. D’Haese, and Anja Verhulst. "Extracellular Nucleotides Regulate Arterial Calcification by Activating Both Independent and Dependent Purinergic Receptor Signaling Pathways." International Journal of Molecular Sciences 21, no. 20 (2020): 7636. http://dx.doi.org/10.3390/ijms21207636.

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Arterial calcification, the deposition of calcium-phosphate crystals in the extracellular matrix, resembles physiological bone mineralization. It is well-known that extracellular nucleotides regulate bone homeostasis raising an emerging interest in the role of these molecules on arterial calcification. The purinergic independent pathway involves the enzymes ecto-nucleotide pyrophosphatase/phosphodiesterases (NPPs), ecto-nucleoside triphosphate diphosphohydrolases (NTPDases), 5′-nucleotidase and alkaline phosphatase. These regulate the production and breakdown of the calcification inhibitor—pyr

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50

Lim, Kenneth, Guerman Molostvov, Maria Lubczanska, et al. "Impaired arterial vitamin D signaling occurs in the development of vascular calcification." PLOS ONE 15, no. 11 (2020): e0241976. http://dx.doi.org/10.1371/journal.pone.0241976.

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Conflicting data exists as to whether vitamin D receptor agonists (VDRa) are protective of arterial calcification. Confounding this, is the inherent physiological differences between human and animal experimental models and our current fragmented understanding of arterial vitamin D metabolism, their alterations in disease states and responses to VDRa’s. Herein, the study aims to address these problems by leveraging frontiers in human arterial organ culture models. Human arteries were collected from a total of 24 patients (healthy controls, n = 12; end-stage CKD, n = 12). Cross-sectional and in

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