Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CALCIFICATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 775 records · Page 43Linked to original sources
PubMed2006

Clinical significance of calcification of the fibrous skeleton of the heart and aortosclerosis in community dwelling elderly. The Cardiovascular Health Study (CHS).

BACKGROUND: Mitral annular calcification (MAC), aortic annular calcification (AAC), and aortic valve sclerosis (AVS) are associated with aging, and MAC and AVS are markers of advanced atherosclerosis. No studies have examined the prevalence and the clinical relevance of all 3 forms of calcification in a single free-living elderly population. METHODS: We used 2-dimensional echocardiography to evaluate MAC, AAC, AVS and all 3 combined in 3929 participants, mean age 76 +/- 5 years, 60% women, in the Cardiovascular Health Study, a prospective community-based observational study designed to assess cardiovascular disease (CVD) risk factors and outcomes in elderly persons. RESULTS: Mitral annular calcification was found in 1640 (42 %) subjects, AAC in 1710 (44 %), AVS in 2114 (54 %), and all 3 combined in 662 (17 %). The participants with these findings were older than those without them, and those with MAC had worse cardiovascular, renal, metabolic, and functional profile than those with AAC and AVS. Age-, sex-, and race-adjusted logistic regression analysis found a significant association between the 3 calcification categories and CVD, the strongest being between the combined group with congestive heart failure (odds ratio 2.04, 95% CI 1.34-3.09). In highly adjusted models, only MAC was associated with CVD, and the strength of association was related to the severity of MAC. CONCLUSIONS: In free-living elderly, MAC, AAC, and AVS are highly prevalent and are associated with CVD. Mitral annular calcification in particular has strong association with CVD, and with an adverse biomedical profile.

Aged↗
PubMed2006

Calcific tendonitis of the subscapularis tendon causing subcoracoid stenosis and coracoid impingement.

Calcific tendonitis is a common disease of the shoulder which usually responds to conservative treatment. In cases unresponsive to conservative management, arthroscopic treatment is sometimes required. While there are several reports on calcifications within the supraspinatus tendon, documented cases involving the subscapularis tendon are rare. We present a case of a 47 year old farmer with recurrent anterior shoulder pain. An MRI revealed calcium deposits as well as a large subcoracoid cyst. Arthroscopic excision of the multiple calcific deposits left a large defect in the subscapularis tendon which was repaired back to the lesser tuberosity using arthroscopic techniques. A coracoplasty resulted in an increased coracohumeral space. The patient followed a conservative postop rehabilitation protocol and ultimately regained full strength and was pain free at the latest follow-up. We postulate two possible etiologies of subscapularis calcific tendonitis: either an idiopathic calcific tendonitis caused a secondary coracoid impingement or a primary subcoracoid stenosis resulted in an interstitial subscapularis tear which eventually resulted in calcium deposition. This report describes the clinical and technical details of arthroscopic excision of calcific deposits of the subscapularis tendon as well as arthroscopic repair of the resulting subscapularis defect.

Arthroscopy↗
PubMed2004

Reduced calcification of bioprostheses, cross-linked via an improved carbodiimide based method.

Glutaraldehyde fixation of bioprosthetic tissue has been used successfully for almost 40 years. However, it is generally recognized that glutaraldehyde fixation of bioprostheses is associated with the occurrence of calcification. Accordingly, many efforts have been undertaken to develop techniques for the fixation of bioprostheses, which will not lead to calcification. Here we describe a new improved carbodiimide based cross-linking method. Rather than cross-linking the tissue through its free primary amine groups, these groups were first blocked with butanal and the tissue was then cross-linked by means of carbodiimide activation of tissue carboxylic acid groups followed by a reaction with a poly(propylene glycol)bis 2-(aminopropyl) ether, (Jeffamine trade mark ). It was demonstrated that cross-linked porcine leaflets had a calcification of less than 1mg/g tissue after 8 weeks sub-dermal implantion in rats. Furthermore, aortic wall calcification was reduced to 50mg/g, compared to standard glutaraldehyde fixed tissue, which showed 120mg/g tissue calcification in the 8 weeks calcification model used.

Animals↗
PubMed2006

Corneal calcification after chemical eye burns caused by eye drops containing phosphate buffer.

PURPOSE: Chemical burns with calcium containing corrosives as well as irrigation with phosphate buffer solutions after eye burns bear the risk of corneal calcification. The aim of this study was to evaluate the correlation between the occurrence of corneal calcification after chemical injuries and the usage of phosphate buffer containing local therapeutics. METHODS: We reviewed the data of 179 patients who have been treated in the University Eye Clinic Aachen, Germany, between 1941 and 2000. Only when the corrosive did not contain calcium and when the initial irrigating solution did not contain phosphate buffer, respectively, were patients included in the study. The cases were analyse, if the patient was treated with phosphate buffer containing eye drops/ointment during the first 7 days of hospitalization or as an out-patient, and if corneal calcification was visible by slit-lamp examination during the follow-up. Statistical analysis was performed using Fischer's exact test. RESULTS: 152 eyes were included. From 63 eyes treated with phosphate buffer containing eye drops, 31 eyes (49%) developed corneal calcification. From 89 eyes treated without phosphate buffer containing eye drops, only 23 eyes (26%) developed corneal calcification. The two-sided p-value of Fischer's exact test is 0.0036. CONCLUSION: During follow-up after chemical eye burns, eye drops containing phosphate buffer double the risk of corneal calcification. We recommend avoiding these agents in order to prevent the burned cornea from additional opacity. Substances containing phosphate buffer are listed in this article.

Buffers↗
PubMedDate not supplied

Inflammatory regulation of extracellular matrix remodeling in calcific aortic valve stenosis.

BACKGROUND: Calcific aortic stenosis (AS), the most frequent heart valve disorder in developed countries, leads to the calcification and fibrous thickening of the valve. While several studies have addressed the process of valvular calcification, the molecular pathomechanisms of the extensive matrix remodeling remain unclear. Because inflammation is present in stenotic valves, we hypothesized that the proinflammatory cytokine tumor necrosis factor alpha (TNFalpha) might influence cell proliferation and regulate the expression and activation of matrix metalloproteinases (MMPs)--enzymes that are thought to be involved in calcific AS. METHODS: Immunohistochemistry for leukocytes, TNFalpha, MMP-1, and the endogenous MMP inhibitor tissue inhibitor of metalloproteinase (TIMP)-1 was performed on human stenotic (n = 19) and control (n = 8) valves. Primary cultures of human aortic valve myofibroblasts were incubated with and without TNFalpha, and cell proliferation was assessed. The expression and activation of MMP-1 were detected by Western blotting and a specific MMP-1 activity assay. RESULTS: Control valves showed scattered macrophages and low expression of TNFalpha, MMP-1, and TIMP-1. In stenotic valves, leukocyte infiltration and a strong, colocalized expression of TNFalpha and MMP-1 were present, while TIMP-1 remained unchanged. Double-label immunofluorescence localized TNFalpha mainly to macrophages. In cultured human aortic valve myofibroblasts, TNFalpha stimulated proliferation and induced a time-dependent increase in MMP-1 expression and activation, while TIMP-1 remained unchanged. CONCLUSION: The results indicate that matrix remodeling in calcific AS involves the expression and activation of MMPs. Activated leukocytes, by the secretion of TNFalpha, may stimulate valvular myofibroblasts to proliferate and express MMPs, thus regulating actively the matrix remodeling in calcific AS.

Aortic Valve Stenosis↗
PubMedDate not supplied

Impact of vessel calcification on outcomes after coronary stenting.

BACKGROUND: Calcified coronary arteries have few viable smooth muscle cells capable of proliferating, and, subsequently, might exhibit less in-stent restenosis. We therefore studied the outcome of stenting in patients with different amounts of coronary calcification. METHODS: Six hundred twenty-one patients who underwent bare metal stenting of calcific native coronary arteries were studied retrospectively. Pre- and postinterventional intravascular ultrasound (IVUS) and qualitative and quantitative coronary angiography (QCA) were performed in 662 lesions. The arc of calcium was measured, and arteries were grouped (A, B, C, and D) according to the calcium arc in IVUS (0-90 degrees , 91-180 degrees , 181-270 degrees , and 271-360 degrees , respectively). Arteries with a superficial calcium arc of < or =270 degrees (Group E) were compared to arteries with >270 degrees calcification (Group F). RESULTS: Clinical and lesion characteristics were similar, and the major complication rate was low (1.9%) in all groups. In Groups A, B, C, and D, patients with more calcific arteries had more non-Q-wave myocardial infarction (MI) (P=.04-.002). Patients in Group F (more extensive superficial calcification) had an increased frequency of non-Q-wave MI compared to Group E. Malapposition of stents to vessel wall and use of rotational atherectomy were more frequent in Group F (P=.001). Late events including death, MI, and revascularization with either coronary artery bypass grafting or percutaneous coronary intervention (PCI) were not different among the groups. Extensive calcification of coronary arteries is associated with more frequent peri-procedural non-Q-wave MI. CONCLUSION: Despite the scarcity of viable cells, the late event rate in severely calcified arteries is not different from mildly calcified arteries. This may be due to more frequent malapposition of stents to vessel wall and augmented trauma during PCI in severely calcified arteries.

Adult↗
PubMed2004

Prevalence of breast arterial calcification in hypertensive patients.

AIM: To determine the age-specific prevalence of breast arterial calcifications in patients with systemic hypertension. METHODS: The mammograms and patient records of 2406 women who underwent screening or diagnostic mammography were reviewed retrospectively. Mammograms were evaluated for the presence of arterial calcification and results were coded. Hypertension was defined as use of anti-hypertensive agents and diabetes was defined as use of oral hypoglycaemic agents or insulin. RESULTS: The prevalence of breast arterial calcification among hypertensives (17.6%) was lower than among diabetics (25.4%). The prevalence in the non-diabetic, non-hypertensive group was lowest (7.3%). The prevalence increased with age in all three groups. The highest prevalence was found in diabetics older than 60 years (81.8%). Breast arterial calcification was not found among women younger than 40 years. CONCLUSION: Breast arterial calcification is associated with hypertension and prevalence increases with age. Breast arterial calcification on mammograms may indicate unsuspected hypertension especially in non-diabetic patients.

Adult↗
PubMed2005

Failure of aneurysm sac shrinkage after endovascular repair; the effect of mural calcification.

AIM: To evaluate the effect of abdominal aortic aneurysm wall calcification on subsequent sac shrinkage after endovascular repair. MATERIALS AND METHODS: Seventy-three patients underwent endovascular aneurysm repair. The degree of sac wall calcification on pre-procedural computed tomography (CT) examination was graded from 1 to 4 according to the degree of circumferential involvement. On follow-up CT imaging, the maximum transverse diameter (MTD) of the sac was recorded, as well as the presence or absence of endoleak. In those patients with a non-shrinking aneurysm, but no CT evidence of endoleak, contrast-enhanced ultrasound (USS) was performed. Any patient with an endoleak, however diagnosed, was excluded from the study. Kruskal-Wallis and Spearman's rank correlation coefficient testing was applied to compare the degree of calcification and change in MTD. RESULTS: Sixty-three pre-procedural CT images were available for calcification grading. Six of this group had endoleaks resulting in 57 sets of data being available for the study. A reduction in MTD occurred in 68.25% of these patients by 1 year post-procedure. Our figures show aortic calcification is inversely associated with MTD reduction at 6 months (p = 0.01), 1 year (p = 0.05) and 2 years (p = 0.05). CONCLUSION: This study indicates that the degree of aortic wall calcification is significant in predicting MTD reduction post-endovascular repair. The possible mechanisms and implications of this are discussed.

Aged↗
PubMed2006

Gas6/Axl-PI3K/Akt pathway plays a central role in the effect of statins on inorganic phosphate-induced calcification of vascular smooth muscle cells.

Apoptosis is essential for the initiation and progression of vascular calcification. Recently, we showed that 3-hydroxy-3-methylglutaryl (HMG) CoA reductase inhibitors (statins) have a protective effect against vascular smooth muscle cell calcification by inhibiting apoptosis, where growth arrest-specific gene 6 (Gas6) plays a pivotal role. In the present study, we clarified the downstream targets of Gas6-mediated survival signaling in inorganic phosphate (Pi)-induced apoptosis and examined the effect of statins. We found that fluvastatin and pravastatin significantly inhibited Pi-induced apoptosis and calcification in a concentration-dependent manner in human aortic smooth muscle cells (HASMC), as was found with atorvastatin previously. Gas6 and its receptor, Axl, expression were downregulated in the presence of Pi, and recombinant human Gas6 (rhGas6) significantly inhibited apoptosis and calcification in a concentration-dependent manner. During apoptosis, Pi suppressed Akt phosphorylation, which was reversed by rhGas6. Wortmannin, a specific phosphatidylinositol 3-OH kinase (PI3K) inhibitor, abolished the increase in Akt phosphorylation by rhGas6 and eliminated the inhibitory effect of rhGas6 on both Pi-induced apoptosis and calcification, suggesting that PI3K-Akt is a downstream signal of the Gas6-mediated survival pathway. Pi reduced phosphorylation of Bcl2 and Bad, and activated caspase 3, all of which were reversed by rhGas6. The inhibitory effect of statins on Pi-induced apoptosis was accompanied by restoration of the Gas6-mediated survival signal pathway: upregulation of Gas6 and Axl expression, increased phosphorylation of Akt and Bcl2, and inhibition of Bad and caspase 3 activation. These findings indicate that the Gas6-mediated survival pathway is the target of statins' effect to prevent vascular calcification.

Androstadienes↗
PubMed2006

Proatherogenic pathways leading to vascular calcification.

Cardiovascular disease is the leading cause of morbidity and mortality in the western world and atherosclerosis is the major common underlying disease. The pathogenesis of atherosclerosis involves local vascular injury, inflammation and oxidative stress as well as vascular calcification. Vascular calcification has long been regarded as a degenerative process leading to mineral deposition in the vascular wall characteristic for late stages of atherosclerosis. However, recent studies identified vascular calcification in early stages of atherosclerosis and its occurrence has been linked to clinical events in patients with cardiovascular disease. Its degree correlates with local vascular inflammation and with the overall impact and the progression of atherosclerosis. Over the last decade, diverse and highly regulated molecular signaling cascades controlling vascular calcification have been described. Local and circulating molecules such as osteopontin, osteoprogerin, leptin and matrix Gla protein were identified as critical regulators of vascular calcification. We here review the current knowledge on molecular pathways of vascular calcification and their relevance for the progression of cardiovascular disease.

Calcinosis↗
PubMed2004

Effect of suprarenal stent struts on the renal artery with ostial calcification observed on CT virtual intravascular endoscopy.

OBJECTIVES: The behaviour of stent struts crossing the renal ostia and their effect on renal ostia configuration is not well understood. The study aims to investigate whether suprarenal stent struts affect the morphological change of the renal artery with ostial calcification observed on CT virtual intravascular endoscopy. METHODS: Nine patients with abdominal aortic aneurysms undergoing suprarenal fixation of stent grafts were included in the study. All patients received a Zenith endovascular graft with uncovered suprarenal components placed above the renal arteries. Renal ostial calcification and configuration of stent wires crossing the renal ostium were characterized in each patient and maximal transverse and longitudinal diameters of the renal ostia were measured on virtual endoscopy pre- and post-stent grafting. RESULTS: There were altogether 17 renal ostia assessed with one patient having atrophic left kidney and no renal ostium being observed. Ostial calcification was found in five of the left renal ostia and five of the right renal ostia with one patient having bilateral ostial calcification. There was no significant difference between the renal ostial diameters measured pre- and post-stent grafting (p>0.05). Suprarenal stent struts were found to cross the renal ostia in various configurations observed on virtual endoscopy. All of the renal arteries were patent on follow-up CT scans after suprarenal fixation without stenosis or occlusion being observed. One patient with atrophic left renal artery developed renal failure following suprarenal stent grafting and received renal dialysis, while in the remaining cases median serum creatinine level did not change significantly. CONCLUSIONS: Suprarenal stent struts did not significantly affect the renal ostia with ostial calcification in terms of the diameter measurements and renal function. Further studies deserve to investigate the long-term effect of stent struts on the renal artery in terms of cross-sectional area reduction caused by stent wires and ostial calcification.

Aged↗
PubMed2004

A comparison of HDL and LDL cholesterol for prevalent coronary calcification.

BACKGROUND: Coronary calcification is a marker for coronary atherosclerosis. It has been postulated that high levels of high density lipoprotein cholesterol (HDL-C) are associated with a reduced amount of atherosclerotic disease while previous reports have found a lack of association between low density lipoprotein cholesterol (LDL-C) and coronary calcification (CAC). The purpose of this study was to compare the correlation and predictive power of HDL-C with LDL-C for prevalent coronary calcification. METHODS: A total of 6093 subjects were studied with respect to coronary calcification, serum cholesterol indices, personal health history and body morphology. Analyses consisted of correlation coefficients, logistic regression and sensitivity analysis to determine the strength of association between HDL-C and coronary calcification after controlling for covariates. RESULTS: The correlation between HDL-C and coronary calcium score (CCS) was three times that of LDL-C. Individuals with an HDL-C level <40 mg/dl had significantly higher calcium scores while increases in HDL-C were associated with a significant reduction in risk for the presence of any calcified plaque. Results of multivariate logistic regression revealed that HDL-C is predictive of calcified plaque development independent of LDL-C. Sensitivities and positive predictive values for both HDL-C and LDL-C were low. CONCLUSIONS: Increasing levels of HDL-C were associated with less coronary calcification and a smaller probability of having any calcified disease supporting the antiatherogenic hypothesis for HDL-C. HDL-C predicts the presence of any calcified atherosclerotic plaque independently of LDL-C. However, neither parameter seems suitable as a screening tool for predicting prevalent calcified atheromatous disease.

Aged↗
PubMed2005

Preliminary experience in the assessment of aortic valve calcification by ECG-gated multislice spiral computed tomography.

BACKGROUND: The aim was to correlate the degree of valvular calcification in patients with aortic stenosis determined by retrospectively electrocardiogram (ECG)-gated multislice spiral computed tomography with stenosis severity assessed by cardiac catheterization. METHODS: Prospective study on 41 patients (18 men, mean age 71+/-8 years) with aortic stenosis, who underwent four detector row multislice spiral computed tomography and cardiac catheterization. Severity of aortic stenosis was classified by cardiac catheterization. Aortic valve area, peak to peak and mean transvalvular gradients were correlated with the degree of calcification determined by multislice spiral computed tomography. Aortic valve calcification was assessed using aortic Agatston score, aortic mass score and aortic volume score. RESULTS: All measured aortic valve calcification scores were significantly higher in patients with severe aortic stenosis (n=29) than in patients with moderate (n=7) or mild aortic stenosis (n=5, p<0.001). Aortic valve calcification scores correlated significantly with aortic valve area (r=-0.49, p=0.001 for aortic mass score) and with peak to peak (r=0.68, p<0.001) and mean (r=0.60, p<0.001) transvalvular gradients. CONCLUSIONS: Severity of aortic valve calcification assessed by cardiac multislice spiral computed tomography is inversely related to aortic valve area and positively correlated with transvalvular gradients. Based on this preliminary data larger studies should be performed with echocardiography as a reference standard in order to validate this new information and its utility in the clinical management of the patient.

Aged↗
PubMed2005

Atherosclerotic calcification and intimal medial thickness of the carotid arteries.

BACKGROUND AND PURPOSE: Carotid intimal medial thickness (IMT) is a measure of subclinical atherosclerosis and is predictive of future cardiovascular events. The purpose of this study was to determine the significance and magnitude of association between IMT and atherosclerotic calcification of the carotid arteries. METHODS: Forty-five subjects underwent electron beam computed tomography of the neck to ascertain the extent of atherosclerotic calcification in the carotid arteries followed by B-mode carotid ultrasonography for IMT. RESULTS: The mean age, BMI and total cholesterol to HDL ratio were 61.4, 26.2 and 4.3, respectively. Forty-one percent were women. The overall mean IMT was 0.91 mm with the mean for the right and left being 0.93 and 0.87 mm, respectively. The median total carotid calcium score (CCS) was 48.4 [range: 0-973]. Age-adjusted correlations were significant between the overall mean IMT and total CCS (r=0.53, p<0.01), mean right IMT and right CCS (0.31, 0.05), mean left IMT and left CCS (0.31, 0.05), right common carotid IMT and right CCS (0.53, <0.01) and left common carotid IMT and left CCS (0.31, 0.05). The mean IMT was 0.14 mm greater in subjects with any carotid calcification adjusted for risk factors. A 0.05 mm increase in the carotid IMT was associated with an approximate 3-fold increase in risk for the presence of atherosclerotic calcification. CONCLUSIONS: Carotid IMT is significantly correlated with and predictive of atherosclerotic calcification. Conversely, individuals with any carotid calcification have significantly greater intimal medial thicknesses.

Aged↗
PubMed2005

Three-dimensional in vivo characterization of calcification in native valves and in Freestyle versus homograft aortic valves.

OBJECTIVE: This article describes a novel interactive method for quantitative evaluation of calcium deposits in the aortic valve by means of electron beam tomography data fusion technique. METHODS: The technique relied on the use of hierarchic 3-dimensional free-form volume registration with fast global optimization between normally acquired and contrast-enhanced electron beam tomographic volume. A total of 66 contrast-enhanced electron beam tomographic scans of the aortic root were performed in 27 patients, 10 with native aortic valve disease (group A) and 17 from a prospective randomized trial of aortic root replacement (group B, 9 Freestyle grafts [Medtronic, Inc, Minneapolis, Minn] and 8 homografts). To validate the in vivo electron beam tomographic measurements, 5 patients from group A underwent electron beam tomographic scans before the operation and then had their own valves, explanted at the time of surgery, analyzed for calcium quantification by ex vivo electron beam tomography. RESULTS: In group A, the mean (+/- SE) calcification score was 6560 +/- 2388, which correlated with peak gradients measured at echocardiography ( r = 0.93, P = .02). In group B, the mean (+/- SE) calcification score was 168 +/- 27, showing a tendency toward a lower calcification for Freestyle valves than for homografts at 2 years after implantation ( P = .052). A mean variability of 6% was found between in vivo electron beam tomographic scores of calcification and those measured on valve specimens after explantation. CONCLUSION: We describe a novel method to characterize the degree and location of calcification in both native valves and postoperative valve implants. The technique may be useful in the management of patients with aortic valve disease and has potential as a screening tool for high-risk patients to diagnose early valve calcification and possibly institute corrective measures.

Aged↗
PubMed2006

Factors influencing calcification of cardiac bioprostheses in adolescent sheep.

OBJECTIVE: We determined the possible effects of age, antimineralization treatments, circulatory implant conditions, prosthesis design, and valve-related structural aspects on valve calcification in adolescent sheep. METHODS: Calcium content was measured by means of atomic absorption spectrometry in bioprostheses implanted in 120 sheep (age <1 year) for a period of 3 or 6 months. RESULTS: Bioprostheses calcified significantly in adolescent sheep, but the extent of calcification was multifactorial. Multivariate analysis of the calcium content reveals that age, mitral or pulmonary implant position, prosthesis design (stented or stentless), structure (porcine or pericardial, wall portion or cusp), and antimineralization treatment are independent factors influencing calcification; implant duration beyond 3 months was not. In juvenile sheep (age 5 months) the wall portion, as well as the cusps of the prosthesis, calcified significantly more than in adolescent sheep (age 11 months). Irrespective of age, the cusps of valves implanted in the mitral position calcified more than those in the pulmonary position. The wall portion of stentless valves calcified more than that of stented valves, and pericardial valves calcified less than porcine valves. The surfactant (Tween 80, No-React, and alpha-amino-oleic acid) and alcohol (ethanol and octanediol) treatment significantly reduced cusp calcification; sodium dodecylsulfate did not. None of the anticalcification treatments was able to prevent wall calcification in stentless porcine valves. CONCLUSION: These findings suggest that tissue valve calcification is determined by many independent factors, which can be identified by using adolescent sheep as a preclinical in vivo model.

Age Factors↗
PubMed2004

Cholestane-3beta, 5alpha, 6beta-triol promotes vascular smooth muscle cells calcification.

Oxysterols found in atherosclerotic plaque may be associated with vascular calcification. We investigated the effect of oxysterol cholestane-3beta, 5alpha, 6beta-triol (Triol) on in vitro calcification of rat vascular smooth muscle cells (VSMCs). In vitro calcification was induced by incubation of VSMCs with beta-glycerophosphate. Calcifying nodule formation, calcium deposition in extracellular matrix, and alkaline phosphatase (ALP) activity were measured as indices of calcification. Because apoptotic bodies can serve as nucleation sites for calcification, apoptosis of calcifying VSMCs was determined by Hoechst 33258 staining, TUNEL, and FITC-labeled annexin V/PI double staining. The calcium deposition and ALP activity in calcifying VSMCs were much higher than those in non-calcifying VSMCs. Triol increased calcifying nodule formation, calcium deposition, ALP activity, and apoptosis of nodular cells in calcifying VSMCs. As determined by 2,7-dichlorofluorescein fluorescence, Triol induced the generation of reactive oxygen species (ROS) in calcifying VSMCs dose- and time-dependently. Triol-induced increases in calcium deposition, ALP activity, apoptosis, and ROS generation were all attenuated by antioxidant vitamin C plus vitamin E (VC + VE). The results demonstrated that Triol promoted VSMCs calcification through direct increase of ALP activity and apoptosis, probably by ROS-related mechanism.

Alkaline Phosphatase↗
PubMed2006

Vascular calcification in uremic conditions: new insights into pathogenesis.

Chronic kidney disease (CKD) patients have an higher incidence of cardiovascular morbidity and mortality compared with the general population. In the past 10 years, several studies pointed out that vascular calcification is a major cause of cardiovascular disease in the dialysis population. In CKD patients, high levels of serum phosphate and parathyroid hormone play a critical role in the pathogenesis of cardiovascular events. Calcium- and aluminum-free phosphate binders provide a new and effective therapeutic tool in preventing cardiovascular calcifications in CKD in animal models and in hemodialysis patients. Moreover, the pathogenesis of vascular and soft-tissue calcification, which traditionally has been associated with a passive calcium-phosphate deposition, certainly also is related to an active, cell-mediated process. In fact, some bone regulatory proteins seem to be able to induce or inhibit mineral deposition in the vasculature. In particular, bone matrix protein 7, alpha2-HS glycoprotein, and matrix GLA protein may be regulatory keys in preventing extraskeletal calcification in uremic conditions. This review presents the current understanding of the pathogenesis of vascular calcification in CKD patients, focusing on these 3 proteins and their protective action on extraskeletal calcification.

Calcinosis↗