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Article ; Online: Cardiovascular Benefits for Blood Donors? A Systematic Review.

Quee, Franke A / Peffer, Karlijn / Ter Braake, Anique D / Van den Hurk, Katja

2022 Volume 36, Issue 3, Page(s) 143–151

Abstract: It has been proposed that blood donation could be protective against cardiovascular disease. The aim of this study is to systematically summarize and evaluate existing observational and experimental studies on effects of blood donation on cardiovascular ... ...

Abstract	It has been proposed that blood donation could be protective against cardiovascular disease. The aim of this study is to systematically summarize and evaluate existing observational and experimental studies on effects of blood donation on cardiovascular risk and disease in donor and general populations. The electronic databases PubMed and EMBASE were searched until March 2019 for experimental and observational studies on blood donation and cardiovascular risk or disease. Excluded were studies performed in patient populations or with controls compared to a patient population, and studies performed in individuals aged <18 or >70. All identified studies were independently screened for eligibility and quality using validated scoring systems by 2 reviewers. A total of 44 studies met all criteria. We included 41 observational studies and 3 experimental studies. 14 studies had a quality assessment score of 7 or higher. Of those, a majority of 9 studies reported a protective effect of blood donation, while 5 studies found no effects on cardiovascular risk factors. Results on other various outcomes were inconsistent and study quality was generally poor. Whether or not blood donation protects against cardiovascular disease remains unclear. Studies showing beneficial effects may have inadequately dealt with the healthy donor effect. High quality studies are lacking and therefore definite conclusions cannot be drawn. Large RCTs or cohort studies of high quality with sufficient follow-up should be conducted to provide evidence on the possible association between blood donation and cardiovascular disease.
MeSH term(s)	Blood Donors ; Cardiovascular Diseases/prevention & control ; Humans ; Observational Studies as Topic
Language	English
Publishing date	2022-04-25
Publishing country	United States
Document type	Journal Article ; Systematic Review ; Research Support, Non-U.S. Gov't
ZDB-ID	639107-2
ISSN	1532-9496 ; 0887-7963
ISSN (online)	1532-9496
ISSN	0887-7963
DOI	10.1016/j.tmrv.2022.04.004
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Zs.A 2239: Show issues

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Article ; Online: Calciprotein Particle Synthesis Strategy Determines In Vitro Calcification Potential.

Zeper, Lara W / Smith, Edward R / Ter Braake, Anique D / Tinnemans, Paul T / de Baaij, Jeroen H F / Hoenderop, Joost G J

Calcified tissue international

2022 Volume 112, Issue 1, Page(s) 103–117

Abstract: ... and D) phosphate and 2.8 mM (CPP-A and B) or 10 mM (CPP-C and D) calcium, with either bovine fetuin ... A (CPP-C) or fetal bovine serum (CPP-A, B and D) as a source of protein, and incubated for 7 (CPP-A2) or ...

Abstract	Circulating calciprotein particles (CPP), colloids of calcium, phosphate and proteins, were identified as potential drivers of the calcification process in chronic kidney disease. The present study compared CPP produced using different protocols with respect to particle morphology, composition, particle number and in vitro calcification potency. CPP were synthesized with 4.4 mM (CPP-A and B) or 6 mM (CPP-C and D) phosphate and 2.8 mM (CPP-A and B) or 10 mM (CPP-C and D) calcium, with either bovine fetuin-A (CPP-C) or fetal bovine serum (CPP-A, B and D) as a source of protein, and incubated for 7 (CPP-A2) or 14 days (CPP-B2), 12 h (CPP-C2, D2 and B1) or 30 min (CPP-D1). Particle number was determined with nanoparticle tracking and calcium content was measured in CPP preparations and to determine human vascular smooth muscle cell (hVSMC) calcification. Morphologically, CPP-C2 were the largest. Particle number did not correspond to the calcium content of CPP. Both methods of quantification resulted in variable potencies of CPP2 to calcify VSMC, with CPP-B2 as most stable inducer of hVSMC calcification. In contrast, CPP-B1 and D1 were unable to induce calcification of hVSMC, and endogenous CPP derived from pooled serum of dialysis patients were only able to calcify hVSMC to a small extent compared to CPP2.CPP synthesized using different protocols appear morphologically similar, but in vitro calcification potency is dependent on composition and how the CPP are quantified. Synthetic CPP are not comparable to endogenous CPP in terms of the calcification propensity.
MeSH term(s)	Humans ; Calcium/metabolism ; Vascular Calcification/metabolism ; Calcification, Physiologic ; Phosphates/metabolism ; Renal Insufficiency, Chronic/metabolism ; alpha-2-HS-Glycoprotein/metabolism
Chemical Substances	Calcium (SY7Q814VUP) ; Phosphates ; alpha-2-HS-Glycoprotein
Language	English
Publishing date	2022-11-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	304266-2
ISSN	1432-0827 ; 0944-0747 ; 0008-0594 ; 0171-967X
ISSN (online)	1432-0827
ISSN	0944-0747 ; 0008-0594 ; 0171-967X
DOI	10.1007/s00223-022-01036-1
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Zs.A 317: Show issues

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Article ; Online: Magnesium to prevent kidney disease-associated vascular calcification: crystal clear?

Ter Braake, Anique D / Vervloet, Marc G / de Baaij, Jeroen H F / Hoenderop, Joost G J

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

2020 Volume 37, Issue 3, Page(s) 421–429

Abstract: Vascular calcification is a prognostic marker for cardiovascular mortality in chronic kidney disease (CKD) patients. In these patients, magnesium balance is disturbed, mainly due to limited ultrafiltration of this mineral, changes in dietary intake and ... ...

Abstract	Vascular calcification is a prognostic marker for cardiovascular mortality in chronic kidney disease (CKD) patients. In these patients, magnesium balance is disturbed, mainly due to limited ultrafiltration of this mineral, changes in dietary intake and the use of diuretics. Observational studies in dialysis patients report that a higher blood magnesium concentration is associated with reduced risk to develop vascular calcification. Magnesium prevents osteogenic vascular smooth muscle cell transdifferentiation in in vitro and in vivo models. In addition, recent studies show that magnesium prevents calciprotein particle maturation, which may be the mechanism underlying the anti-calcification properties of magnesium. Magnesium is an essential protective factor in the calcification milieu, which helps to restore the mineral-buffering system that is overwhelmed by phosphate in CKD patients. The recognition that magnesium is a modifier of calciprotein particle maturation and mineralization of the extracellular matrix renders it a promising novel clinical tool to treat vascular calcification in CKD. Consequently, the optimal serum magnesium concentration for patients with CKD may be higher than in the general population.
MeSH term(s)	Humans ; Magnesium/therapeutic use ; Phosphates/therapeutic use ; Renal Dialysis ; Renal Insufficiency, Chronic/complications ; Renal Insufficiency, Chronic/therapy ; Vascular Calcification/etiology ; Vascular Calcification/prevention & control
Chemical Substances	Phosphates ; Magnesium (I38ZP9992A)
Language	English
Publishing date	2020-12-26
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	90594-x
ISSN	1460-2385 ; 0931-0509
ISSN (online)	1460-2385
ISSN	0931-0509
DOI	10.1093/ndt/gfaa222
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Zs.A 2198: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Magnesium Counteracts Vascular Calcification: Passive Interference or Active Modulation?

Ter Braake, Anique D / Shanahan, Catherine M / de Baaij, Jeroen H F

Arteriosclerosis, thrombosis, and vascular biology

2017 Volume 37, Issue 8, Page(s) 1431–1445

Abstract: Over the last decade, an increasing number of studies report a close relationship between serum magnesium concentration and cardiovascular disease risk in the general population. In end-stage renal disease, an association was found between serum ... ...

Abstract	Over the last decade, an increasing number of studies report a close relationship between serum magnesium concentration and cardiovascular disease risk in the general population. In end-stage renal disease, an association was found between serum magnesium and survival. Hypomagnesemia was identified as a strong predictor for cardiovascular disease in these patients. A substantial body of in vitro and in vivo studies has identified a protective role for magnesium in vascular calcification. However, the precise mechanisms and its contribution to cardiovascular protection remain unclear. There are currently 2 leading hypotheses: first, magnesium may bind phosphate and delay calcium phosphate crystal growth in the circulation, thereby passively interfering with calcium phosphate deposition in the vessel wall. Second, magnesium may regulate vascular smooth muscle cell transdifferentiation toward an osteogenic phenotype by active cellular modulation of factors associated with calcification. Here, the data supporting these major hypotheses are reviewed. The literature supports both a passive inorganic phosphate-buffering role reducing hydroxyapatite formation and an active cell-mediated role, directly targeting vascular smooth muscle transdifferentiation. However, current evidence relies on basic experimental designs that are often insufficient to delineate the underlying mechanisms. The field requires more advanced experimental design, including determination of intracellular magnesium concentrations and the identification of the molecular players that regulate magnesium concentrations in vascular smooth muscle cells.
MeSH term(s)	Animals ; Calcium Phosphates/metabolism ; Cell Transdifferentiation ; Female ; Homeostasis ; Humans ; Intestines/metabolism ; Kidney/metabolism ; Kidney/physiopathology ; Magnesium/blood ; Male ; Muscle, Smooth, Vascular/metabolism ; Muscle, Smooth, Vascular/pathology ; Myocytes, Smooth Muscle/metabolism ; Myocytes, Smooth Muscle/pathology ; Osteogenesis ; Phenotype ; Prognosis ; Renal Insufficiency, Chronic/blood ; Renal Insufficiency, Chronic/complications ; Renal Insufficiency, Chronic/physiopathology ; Risk Factors ; Vascular Calcification/blood ; Vascular Calcification/etiology ; Vascular Calcification/pathology
Chemical Substances	Calcium Phosphates ; calcium phosphate (97Z1WI3NDX) ; Magnesium (I38ZP9992A)
Language	English
Publishing date	2017-08
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.117.309182
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Zs.A 1705: Show issues

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Article ; Online: Low plasma magnesium concentration and future abdominal aortic calcifications in moderate chronic kidney disease.

Ter Braake, Anique D / Govers, Larissa P / Peeters, Mieke J / van Zuilen, Arjan D / Wetzels, Jack F M / Blankenstijn, Peter J / Hoenderop, Joost G J / de Baaij, Jeroen H F / van den Brand, Jan A J G

BMC nephrology

2021 Volume 22, Issue 1, Page(s) 71

Abstract: Background: Higher plasma magnesium concentrations are associated with reduced cardiovascular disease risk in chronic kidney disease (CKD) patients. The importance of plasma magnesium concentration for vascular calcification in earlier stages of CKD ... ...

Abstract	Background: Higher plasma magnesium concentrations are associated with reduced cardiovascular disease risk in chronic kidney disease (CKD) patients. The importance of plasma magnesium concentration for vascular calcification in earlier stages of CKD remains underexplored. This study investigated whether plasma magnesium is a determinant for the presence and severity of vascular calcification in moderate CKD. Methods: Retrospective analysis was performed using abdominal aortic calcification (AAC) scores in 280 patients with stage 3 and 4 CKD enrolled in the MASTERPLAN trial. Lateral abdominal X-ray was used to evaluate AAC. Plasma magnesium concentration were measured over time. A zero-inflated Poisson model determined the association between plasma magnesium concentration and AAC. Results: 79 out of 280 patients did not have AAC, and in patients with AAC the median calcification score was 3.5 (interquartile range: 0.0-8.6). The mean plasma magnesium concentration was 0.76 ± 0.10 mmol/L at baseline. A 0.1 mmol/L higher plasma magnesium concentration was associated with lower AAC of 0.07 point (95% CI -0.28 - 0.14). A 0.1 mmol/L higher plasma magnesium lowered the odds of detecting any AAC by 30% (OR = 0.63; 95% CI 0.29-1.37). After 1 year and 4 years (at time of X-ray) of follow-up this association was attenuated (OR = 0.93; 95% CI 0.61-1.43 and 0.93; 95% CI 0.60-1.45, respectively). None of these associations reached statistical significance. Conclusions: Plasma magnesium concentration at baseline is not associated with the risk for future AAC. Interventions increasing magnesium to avoid vascular calcification may have greatest potential in early CKD stages prior to onset of vascular calcification.
MeSH term(s)	Adult ; Aged ; Aorta, Abdominal ; Aortic Diseases/etiology ; Female ; Humans ; Magnesium/blood ; Male ; Middle Aged ; Renal Insufficiency, Chronic/blood ; Renal Insufficiency, Chronic/complications ; Retrospective Studies ; Severity of Illness Index ; Vascular Calcification/etiology
Chemical Substances	Magnesium (I38ZP9992A)
Language	English
Publishing date	2021-02-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2041348-8
ISSN	1471-2369 ; 1471-2369
ISSN (online)	1471-2369
ISSN	1471-2369
DOI	10.1186/s12882-021-02267-4
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Article ; Online: Magnesium prevents vascular calcification in vitro by inhibition of hydroxyapatite crystal formation.

Ter Braake, Anique D / Tinnemans, Paul T / Shanahan, Catherine M / Hoenderop, Joost G J / de Baaij, Jeroen H F

Scientific reports

2018 Volume 8, Issue 1, Page(s) 2069

Abstract: Magnesium has been shown to effectively prevent vascular calcification associated with chronic kidney disease. Magnesium has been hypothesized to prevent the upregulation of osteoblastic genes that potentially drives calcification. However, extracellular ...

Abstract	Magnesium has been shown to effectively prevent vascular calcification associated with chronic kidney disease. Magnesium has been hypothesized to prevent the upregulation of osteoblastic genes that potentially drives calcification. However, extracellular effects of magnesium on hydroxyapatite formation are largely neglected. This study investigated the effects of magnesium on intracellular changes associated with transdifferentiation and extracellular crystal formation. Bovine vascular smooth muscle cells were calcified using β-glycerophosphate. Transcriptional analysis, alkaline phosphatase activity and detection of apoptosis were used to identify transdifferentiation. Using X-ray diffraction and energy dispersive spectroscopy extracellular crystal composition was investigated. Magnesium prevented calcification in vascular smooth muscle cells. β-glycerophosphate increased expression of osteopontin but no other genes related to calcification. Alkaline phosphatase activity was stable and apoptosis was only detected after calcification independent of magnesium. Blocking of the magnesium channel TRPM7 using 2-APB did not abrogate the protective effects of magnesium. Magnesium prevented the formation of hydroxyapatite, which formed extensively during β-glycerophosphate treatment. Magnesium reduced calcium and phosphate fractions of 68% and 41% extracellular crystals, respectively, without affecting the fraction of magnesium. This study demonstrates that magnesium inhibits hydroxyapatite formation in the extracellular space, thereby preventing calcification of vascular smooth muscle cells.
MeSH term(s)	Alkaline Phosphatase/genetics ; Alkaline Phosphatase/metabolism ; Animals ; Apoptosis ; Boron Compounds/pharmacology ; Cattle ; Cells, Cultured ; Durapatite/metabolism ; Glycerophosphates/pharmacology ; Magnesium/pharmacology ; Muscle, Smooth, Vascular/cytology ; Myocytes, Smooth Muscle/drug effects ; Myocytes, Smooth Muscle/metabolism ; Osteopontin/genetics ; Osteopontin/metabolism ; TRPM Cation Channels/antagonists & inhibitors ; Vascular Calcification/metabolism
Chemical Substances	Boron Compounds ; Glycerophosphates ; TRPM Cation Channels ; Osteopontin (106441-73-0) ; Durapatite (91D9GV0Z28) ; 2-aminoethoxydiphenyl borate (E4ES684O93) ; Alkaline Phosphatase (EC 3.1.3.1) ; Magnesium (I38ZP9992A) ; beta-glycerophosphoric acid (WWH06G87W6)
Language	English
Publishing date	2018-02-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-20241-3
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Article ; Online: Magnesium prevents vascular calcification in Klotho deficiency.

Ter Braake, Anique D / Smit, Anna E / Bos, Caro / van Herwaarden, Antonius E / Alkema, Wynand / van Essen, Huib W / Bravenboer, Nathalie / Vervloet, Marc G / Hoenderop, Joost G J / de Baaij, Jeroen H F

Kidney international

2019 Volume 97, Issue 3, Page(s) 487–501

Abstract: ... parathyroid hormone, 1,25-dihydroxyvitamin D ...

Abstract	Klotho knock-out mice are an important model for vascular calcification, which is associated with chronic kidney disease. In chronic kidney disease, serum magnesium inversely correlates with vascular calcification. Here we determine the effects of serum magnesium on aortic calcification in Klotho knock-out mice treated with a minimal or a high magnesium diet from birth. After eight weeks, serum biochemistry and aorta and bone tissues were studied. Protective effects of magnesium were characterized by RNA-sequencing of the aorta and micro-CT analysis was performed to study bone integrity. A high magnesium diet prevented vascular calcification and aortic gene expression of Runx2 and matrix Gla protein found in such mice on the minimal magnesium diet. Differential expression of inflammation and extracellular matrix remodeling genes accompanied the beneficial effects of magnesium on calcification. High dietary magnesium did not affect serum parathyroid hormone, 1,25-dihydroxyvitamin D
MeSH term(s)	Animals ; Glucuronidase/deficiency ; Glucuronidase/genetics ; Klotho Proteins ; Magnesium/pharmacology ; Mice ; Mice, Knockout ; Parathyroid Hormone ; Phosphates ; Renal Insufficiency, Chronic ; Vascular Calcification/genetics ; Vascular Calcification/prevention & control
Chemical Substances	Parathyroid Hormone ; Phosphates ; Glucuronidase (EC 3.2.1.31) ; Klotho Proteins (EC 3.2.1.31) ; Magnesium (I38ZP9992A)
Language	English
Publishing date	2019-11-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2019.09.034
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Zs.A 797: Show issues

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Article ; Online: Calciprotein particle inhibition explains magnesium-mediated protection against vascular calcification.

Ter Braake, Anique D / Eelderink, Coby / Zeper, Lara W / Pasch, Andreas / Bakker, Stephan J L / de Borst, Martin H / Hoenderop, Joost G J / de Baaij, Jeroen H F

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

2019 Volume 35, Issue 5, Page(s) 765–773

Abstract: Background: Phosphate (Pi) toxicity is a strong determinant of vascular calcification development in chronic kidney disease (CKD). Magnesium (Mg2+) may improve cardiovascular risk via vascular calcification. The mechanism by which Mg2+ counteracts ... ...

Abstract	Background: Phosphate (Pi) toxicity is a strong determinant of vascular calcification development in chronic kidney disease (CKD). Magnesium (Mg2+) may improve cardiovascular risk via vascular calcification. The mechanism by which Mg2+ counteracts vascular calcification remains incompletely described. Here we investigated the effects of Mg2+ on Pi and secondary crystalline calciprotein particles (CPP2)-induced calcification and crystal maturation. Methods: Vascular smooth muscle cells (VSMCs) were treated with high Pi or CPP2 and supplemented with Mg2+ to study cellular calcification. The effect of Mg2+ on CPP maturation, morphology and composition was studied by medium absorbance, electron microscopy and energy dispersive spectroscopy. To translate our findings to CKD patients, the effects of Mg2+ on calcification propensity (T50) were measured in sera from CKD patients and healthy controls. Results: Mg2+ supplementation prevented Pi-induced calcification in VSMCs. Mg2+ dose-dependently delayed the maturation of primary CPP1 to CPP2 in vitro. Mg2+ did not prevent calcification and associated gene and protein expression when added to already formed CPP2. Confirmatory experiments in human serum demonstrated that the addition of 0.2 mmol/L Mg2+ increased T50 from healthy controls by 51 ± 15 min (P < 0.05) and CKD patients by 44 ± 13 min (P < 0.05). Each further 0.2 mmol/L addition of Mg2+ led to further increases in both groups. Conclusions: Our results demonstrate that crystalline CPP2 mediates Pi-induced calcification in VSMCs. In vitro, Mg2+ delays crystalline CPP2 formation and thereby prevents Pi-induced calcification.
MeSH term(s)	Calcium Phosphates/metabolism ; Cells, Cultured ; Dietary Supplements ; Humans ; Magnesium/pharmacology ; Myocytes, Smooth Muscle/drug effects ; Myocytes, Smooth Muscle/metabolism ; Vascular Calcification/metabolism ; Vascular Calcification/prevention & control ; alpha-2-HS-Glycoprotein/metabolism
Chemical Substances	AHSG protein, human ; Calcium Phosphates ; alpha-2-HS-Glycoprotein ; Magnesium (I38ZP9992A)
Language	English
Publishing date	2019-11-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	90594-x
ISSN	1460-2385 ; 0931-0509
ISSN (online)	1460-2385
ISSN	0931-0509
DOI	10.1093/ndt/gfz190
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Zs.A 2198: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Magnesium prevents vascular calcification in vitro by inhibition of hydroxyapatite crystal formation

Anique D. ter Braake / Paul T. Tinnemans / Catherine M. Shanahan / Joost G. J. Hoenderop / Jeroen H. F. de Baaij

Scientific Reports, Vol 8, Iss 1, Pp 1-

2018 Volume 11

Abstract: Abstract Magnesium has been shown to effectively prevent vascular calcification associated with chronic kidney disease. Magnesium has been hypothesized to prevent the upregulation of osteoblastic genes that potentially drives calcification. However, ... ...

Abstract	Abstract Magnesium has been shown to effectively prevent vascular calcification associated with chronic kidney disease. Magnesium has been hypothesized to prevent the upregulation of osteoblastic genes that potentially drives calcification. However, extracellular effects of magnesium on hydroxyapatite formation are largely neglected. This study investigated the effects of magnesium on intracellular changes associated with transdifferentiation and extracellular crystal formation. Bovine vascular smooth muscle cells were calcified using β-glycerophosphate. Transcriptional analysis, alkaline phosphatase activity and detection of apoptosis were used to identify transdifferentiation. Using X-ray diffraction and energy dispersive spectroscopy extracellular crystal composition was investigated. Magnesium prevented calcification in vascular smooth muscle cells. β-glycerophosphate increased expression of osteopontin but no other genes related to calcification. Alkaline phosphatase activity was stable and apoptosis was only detected after calcification independent of magnesium. Blocking of the magnesium channel TRPM7 using 2-APB did not abrogate the protective effects of magnesium. Magnesium prevented the formation of hydroxyapatite, which formed extensively during β-glycerophosphate treatment. Magnesium reduced calcium and phosphate fractions of 68% and 41% extracellular crystals, respectively, without affecting the fraction of magnesium. This study demonstrates that magnesium inhibits hydroxyapatite formation in the extracellular space, thereby preventing calcification of vascular smooth muscle cells.
Keywords	Medicine ; R ; Science ; Q
Subject code	600
Language	English
Publishing date	2018-02-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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