ライフサイエンスコーパス: vascular calcification

1 Gla protein (MGP) have been correlated with vascular calcification.

2 ase (CKD) despite progression of accelerated vascular calcification.

3 owever, they also promote the progression of vascular calcification.

4 ight be a risk factor for the development of vascular calcification.

5 abolism is common in CKD patients and drives vascular calcification.

6 d protection from factors known to stimulate vascular calcification.

7 to the mechanisms underlying atherosclerotic vascular calcification.

8 ) plays an important role in atherosclerotic vascular calcification.

9 rophosphate, another endogenous inhibitor of vascular calcification.

10 entiation and bone formation are involved in vascular calcification.

11 ated in patients with CN and plays a role in vascular calcification.

12 ting a promising target for the treatment of vascular calcification.

13 tors of mineral metabolism and inhibitors of vascular calcification.

14 sis, release and functions within and beyond vascular calcification.

15 Here, we have examined the role of FXR in vascular calcification.

16 est that osteoprotegerin may protect against vascular calcification.

17 Relatively little is known about noncoronary vascular calcification.

18 chondrogenic" profile has been implicated in vascular calcification.

19 e BMP binding is essential for prevention of vascular calcification.

20 pericardial fat, metabolic risk factors, and vascular calcification.

21 d other studies that suggest that they cause vascular calcification.

22 icalcitol may protect against CKD-stimulated vascular calcification.

23 crease risk and complicate the management of vascular calcification.

24 rphosphatemia is an important contributor to vascular calcification.

25 is that exogenous androgen treatment induces vascular calcification.

26 fetuin, and osteopontin, also contribute to vascular calcification.

27 ence suggests that they could participate in vascular calcification.

28 ences of prolonged glucocorticoid therapy on vascular calcification.

29 y program is upregulated in association with vascular calcification.

30 , we will discuss the actions of the BMPs in vascular calcification.

31 of bone and spinal and other ligaments, and vascular calcification.

32 died than BMP-2 may have opposing actions in vascular calcification.

33 he presence of vascular (18)F-FDG uptake and vascular calcification.

34 rocess thought critical in the initiation of vascular calcification.

35 Dalcetrapib therapy did not affect vascular calcification.

36 between MMP-mediated elastin degradation and vascular calcification.

37 h early success in preventing progression of vascular calcification.

38 sel wall may be important in the etiology of vascular calcification.

39 ate its efficacy as a potential treatment of vascular calcification.

40 emia and have been associated with increased vascular calcification.

41 age by BMP2-Msx2 signaling and contribute to vascular calcification.

42 k, suggesting an inhibitory effect of OPN in vascular calcification.

43 levant therapeutic targets for mitigation of vascular calcification.

44 injury dramatically reduced the severity of vascular calcification.

45 erging during the past year in regulation of vascular calcification.

46 erlipidemia and atherogenic phospholipids in vascular calcification.

47 investigate the molecular mechanisms driving vascular calcification.

48 uggest a positive role for SMCs in promoting vascular calcification.

49 st and ankle periarticular calcification and vascular calcification.

50 vestigated the role of TNF-alpha in in vitro vascular calcification.

51 dy, we investigated the role of apoptosis in vascular calcification.

52 n smooth muscle cell (HSMC) culture model of vascular calcification.

53 es including restenosis, atherosclerosis and vascular calcification.

54 nt an adaptive mechanism aimed at preventing vascular calcification.

55 not develop obesity, diabetes, atheroma, or vascular calcification.

56 new therapeutic targets in the management of vascular calcification.

57 ascular diseases such as atherosclerosis and vascular calcification.

58 new approaches to developing treatments for vascular calcification.

59 8:0-PA) mediate SFA-induced lipotoxicity and vascular calcification.

60 tment of rare and common diseases of ectopic vascular calcification.

61 rating that PDK4 is a therapeutic target for vascular calcification.

62 ascular diseases such as atherosclerosis and vascular calcification.

63 gesting that PDK4 plays an important role in vascular calcification.

64 key lipogenic pathway in SMCs that mediates vascular calcification.

65 characteristic events in the development of vascular calcification.

66 osphorylation and activation, thus promoting vascular calcification.

67 x Gla protein (MGP) is a potent inhibitor of vascular calcification.

68 egenerative cardiovascular disease including vascular calcification.

69 osteodystrophy, and prevented CKD-stimulated vascular calcification.

70 esigning methods to improve defenses against vascular calcification.

71 be potential therapies for the treatment of vascular calcification.

72 m to contribute osteoprogenitor cells to the vascular calcification.

73 ation of pyrophosphate, a major inhibitor of vascular calcification.

74 animals had an impaired capacity to inhibit vascular calcification.

75 uction, and AAA formation without disturbing vascular calcification.

76 encing coronary heart disease and attenuates vascular calcification.

77 ic inflammation, endothelial dysfunction and vascular calcifications.

78 celerated aging that includes osteopenia and vascular calcifications.

79 ons have also been correlated with increased vascular calcification, a hallmark of atherosclerotic an

80 Vascular calcification, a pathologic response to defecti

81 establish the role of fibroblasts in medial vascular calcification, a pathological process known to

82 mputed tomography-based measures of valvular/vascular calcification, adiposity, and muscle attenuatio

83 ders on parameters of mineral metabolism and vascular calcification among patients with moderate to a

84 ht to contribute to extraskeletal (including vascular) calcification among patients with chronic kidn

85 e reabsorption in the kidney and counteracts vascular calcification and aging.

86 PTH(1-34) inhibits vascular calcification and aortic osteogenic differentia

87 gible for statins by ACC/AHA guidelines with vascular calcification and at low to intermediate ASCVD

88 ism but also possibly to reduce the risk for vascular calcification and cardiovascular mortality.

89 potential implications for the mechanisms of vascular calcification and for the development of novel

90 lays a causative role in the pathogenesis of vascular calcification and generated mice with SMC-speci

91 betes mellitus, is associated with increased vascular calcification and increased modification of pro

92 ing water (0.28 M) prevented soft tissue and vascular calcification and increased the life span of kl

93 This study investigated noncoronary vascular calcification and its influence on changes in v

94 activity, which is instrumental in promoting vascular calcification and may be limited by increasing

95 serum phosphate levels have been linked with vascular calcification and mortality among dialysis pati

96 sease is highlighted by significant residual vascular calcification and mortality in Mgp(-/-);Tgm2(-/

97 m and atherosclerotic plaques that regulates vascular calcification and neointimal formation, and inh

98 The common association between vascular calcification and osteoporosis suggests a link

99 onal role of SMC-derived Runx2 in regulating vascular calcification and promoting infiltration of mac

100 hese tests are inaccurate in the settings of vascular calcification and small-vessel disease.

101 ifications may contribute to the severity of vascular calcification and suggests that therapy should

102 ferentiation is an important process driving vascular calcification and the appearance of skeletal el

103 ole of protein O-GlcNAcylation in regulating vascular calcification and the underlying mechanisms.

104 Vascular calcification and vascular metabolic activity r

105 at have been associated with soft tissue and vascular calcification and with adverse cardiovascular o

106 removes O-GlcNAcylation, further accelerated vascular calcification and worsened aortic compliance of

107 Klotho, first, as an endogenous inhibitor of vascular calcification and, second, as a cofactor requir

108 ssary to reduce significantly the accrual of vascular calcifications and cardiovascular mortality in

109 tional therapy should be initiated to reduce vascular calcifications and cardiovascular mortality?

110 itamin D activity, is the major stimulus for vascular calcifications and contributes to the increased

111 and excessive vitamin D activity, as well as vascular calcifications and mortality in FGF23 null mice

112 P1-Fc fusion protein prevents the mortality, vascular calcifications and sequela of disease in animal

113 idence of degenerative arthritis, frostbite, vascular calcification, and adaptation to cultural and g

114 sents an extreme model for arteriosclerosis, vascular calcification, and bone disorders, all of which

115 to hyperthyroidism, metabolic bone disease, vascular calcification, and cardiovascular mortality.

116 CKD-MBD is characterized by osteodystrophy, vascular calcification, and stimulation of osteocyte sec

117 uggest that N-3 fatty acids directly inhibit vascular calcification, and that the inhibitory effects

118 One third of the patients had retinopathy or vascular calcifications, and 24% had diabetes.

119 t corrected the hyperphosphatemia, prevented vascular calcifications, and rescued the lethal phenotyp

120 5-dihydroxyvitamin D3 [1,25(OH)(2)D] levels; vascular calcifications; and early death.

121 The mechanisms involved in the initiation of vascular calcification are not known, but matrix vesicle

122 ed that the extent and histoanatomic type of vascular calcification are predictors of subsequent vasc

123 he mechanism by which phosphorous stimulates vascular calcification, as well as how controlling hyper

124 contribution of the extracellular matrix in vascular calcification associated with chronic kidney di

125 ciency, and restoration of Klotho attenuates vascular calcification associated with CKD.

126 dentify two potential therapeutic targets in vascular calcification associated with MGP dysfunction a

127 ix Gla protein (MGP), osteopontin (OPN), and vascular calcification-associated factor (VCAF) mRNAs.

128 The presence of vascular calcification at baseline is associated with pr

129 and PO(4)(3-) are not sufficient for medial vascular calcification because of inhibition by pyrophos

130 with chronic kidney disease are at risk for vascular calcification because of multiple risk factors

131 Recent studies have shown that induction of vascular calcification begins in early normophosphatemic

132 Matrix Gla protein (MGP) is an inhibitor of vascular calcification but its mechanism of action and p

133 have shown that vitamin K treatment reduced vascular calcification, but human data are limited.

134 gest that the cAMP pathway promotes in vitro vascular calcification by enhancing osteoblast-like diff

135 Klotho ameliorates vascular calcification by enhancing phosphaturia, preser

136 Uremic animals had increased vascular calcification by histology and chemical analysi

137 ults show that upregulation of PDK4 promotes vascular calcification by increasing osteogenic markers

138 lts suggest that TNF-alpha enhances in vitro vascular calcification by promoting osteoblastic differe

139 pothesized that HDL may also protect against vascular calcification by regulating the osteogenic acti

140 Whether or not vascular calcification can be reversed is not yet known,

141 entral role in regulating the development of vascular calcification coincident with declines in skele

142 Vascular calcification contributes to the high risk of c

143 s and osteoprotegerin (OPG) protects against vascular calcification, define how OPG genetic polymorph

144 Vascular calcification develops within atherosclerotic l

145 Patients with ESRD experience accelerated vascular calcification, due at least in part to dysregul

146 ontrol to avoid bone loss (insufficiency) or vascular calcification (excess).

147 cuss current understanding of the process of vascular calcification, focusing specifically on the dis

148 One key contributor to this mortality is vascular calcification, for which no therapy currently e

149 h the mechanism and clinical consequences of vascular calcification, future therapeutic strategies ma

150 A link between bone and vascular calcification has been shown.

151 signaling that regulates the development of vascular calcification has not been investigated in dept

152 ctive role of OPG, in animal models, against vascular calcification has not been replicated in human

153 y a passive process of dead and dying cells, vascular calcification has now emerged as a highly regul

154 recent years, several mechanisms to explain vascular calcification have been identified including (1

155 Hyperphosphatemia and vascular calcification have emerged as cardiovascular ri

156 ontributes to disordered mineral metabolism, vascular calcification, impaired kidney function, and bo

157 Vascular calcification impairs vessel compliance and inc

158 7 ameliorates chronic kidney disease induced-vascular calcification in 5/6 nephrectomized ApoE(-/-) m

159 with cardiovascular disease risk factors and vascular calcification in a community-based sample are l

160 erphosphatemia is thought to underlie medial vascular calcification in advanced renal failure, but ca

161 The process of tunica media vascular calcification in CKD appears to involve a pheno

162 No longer can we accept the concept that vascular calcification in CKD is a passive process resul

163 The mechanism of vascular calcification in CKD is not understood fully, b

164 herapies to limit the destructive effects of vascular calcification in CKD patients.

165 BMP-7 also reverses vascular calcification in CKD, and reduction in vascular

166 synergistic, providing a major stimulus for vascular calcification in CKD.

167 del to explain the pathway of development of vascular calcification in CKD.

168 tive effect of O-GlcNAcylation in regulating vascular calcification in diabetes mellitus and uncovere

169 t altered PPi metabolism could contribute to vascular calcification in hemodialysis patients.

170 investigate mechanisms that cause excessive vascular calcification in HGPS.

171 Excessive vascular calcification in Lmna(G609G) mice is caused by

172 fferentiation of VSMC in the pathogenesis of vascular calcification in mice and defined the functiona

173 process in HGPS that may also contribute to vascular calcification in normal aging, because progerin

174 sk was modestly attenuated by adjustment for vascular calcification in other vascular beds, suggestin

175 laborated an osteogenic milieu that promotes vascular calcification in part via paracrine Wnt signals

176 ts in our understanding of the mechanisms of vascular calcification in patients with early CKD requir

177 multiple factors and mechanisms involved in vascular calcification in patients with kidney disease,

178 , while calciphylaxis of CKD is a ubiquitous vascular calcification in patients with renal failure.

179 oronary artery disease, atherosclerosis, and vascular calcification in patients.

180 Treatment with pyrophosphate inhibited vascular calcification in progeroid mice.

181 ned in cultured rat aortas and in a model of vascular calcification in rats with renal failure.

182 hat can increase exosome release can promote vascular calcification in response to environmental calc

183 lain the observed high clinical incidence of vascular calcification in the osteoporotic patient popul

184 t it would also be an effective treatment of vascular calcification in this setting.

185 rmation and has been shown to inhibit medial vascular calcification in vitamin D-toxic rats.

186 onstrate that signaling through Axl inhibits vascular calcification in vitro and suggest that therape

187 ies suggest that BASMCs can be used to model vascular calcification in vitro and that soluble osteopo

188 Warfarin can stimulate vascular calcification in vitro via activation of beta-c

189 To determine whether these cells modulate vascular calcification in vitro, calcifying vascular cel

190 of intact human vessels, factors initiating vascular calcification in vivo and the role of calcium a

191 The relevance of these in vitro findings to vascular calcification in vivo was further studied in ma

192 High-fat-diet-induced vascular calcification in vivo was markedly inhibited in

193 ay open up new avenues for the prevention of vascular calcification in vivo.

194 correct either the hyperphosphatemia or the vascular calcifications in FGF23 null mice, indicating t

195 2)D and calcium are not sufficient to induce vascular calcifications in the absence of hyperphosphate

196 maging techniques are available to visualize vascular calcification, including fluoroscopy, echocardi

197 lar smooth muscle cells (VSMCs) that promote vascular calcification, including stimulation of osteoge

198 Vascular calcification increasingly afflicts our aging,

199 radiated atherosclerotic mice did not affect vascular calcification, indicating a primary role of SMC

200 and despite persistent hyperphosphatemia and vascular calcifications, indicating that excessive vitam

201 w beta-catenin-targeting strategy to prevent vascular calcification induced by warfarin and identify

202 Vascular calcification initiates with matrix vesicle for

203 Vascular calcification is a common complication in ather

204 Vascular calcification is a common complication in CKD,

205 Vascular calcification is a common feature of major card

206 Vascular calcification is a common finding in atheroscle

207 Vascular calcification is a common problem among the eld

208 Vascular calcification is a complex biological process t

209 f calcium and phosphate, it now appears that vascular calcification is a consequence of tightly regul

210 Vascular calcification is a frequent cause of morbidity

211 worldwide have converged to demonstrate that vascular calcification is a highly regulated form of bio

212 Vascular calcification is a highly regulated process inv

213 Vascular calcification is a highly regulated process tha

214 Vascular calcification is a major contributor to cardiov

215 Vascular calcification is a major contributor to the pro

216 Vascular calcification is a major risk factor for cardio

217 Vascular calcification is a predictor of cardiovascular

218 RATIONALE: Vascular calcification is a process similar to bone form

219 Vascular calcification is a regulated process that invol

220 Vascular calcification is a serious cardiovascular compl

221 Widespread vascular calcification is a ubiquitous feature of aging

222 The etiology of vascular calcification is also increasingly recognized a

223 Vascular calcification is an active cell-mediated proces

224 Vascular calcification is an ectopic calcification that

225 Vascular calcification is associated with an increased r

226 Vascular calcification is associated with cardiovascular

227 Vascular calcification is common in chronic kidney disea

228 Our studies suggest that the development of vascular calcification is coupled with the formation of

229 cular calcification in CKD, and reduction in vascular calcification is due, in part, to reduced serum

230 Vascular calcification is highly associated with cardiov

231 Vascular calcification is highly correlated with cardiov

232 Vascular calcification is known to be a risk factor for

233 Although the role of BMP-2 in vascular calcification is not proven, it has been the mo

234 axis, and idiopathic arterial calcification, vascular calcification is now recognized as a marker of

235 Vascular calcification is present in many pathological c

236 Vascular calcification is prevalent in aging as well as

237 Vascular calcification is prevalent in the aging populat

238 Vascular calcification is recognized as an independent p

239 The extent to which vascular calcification is reversible and the possible me

240 Vascular calcification is strongly linked with increased

241 ar pathways control both bone remodeling and vascular calcification is widely accepted, but the preci

242 prevention and/or therapeutic strategies for vascular calcification, it is important to understand th

243 alcification, leading to the suggestion that vascular calcification may be a regulated process with s

244 and calcification of vascular cells and that vascular calcification may be another target of HDL acti

245 Risk conferred by parental premature CVD on vascular calcification may be mediated through novel mec

246 t soluble osteopontin released near sites of vascular calcification may represent an adaptive mechani

247 In this study, we use 2 mouse models of vascular calcification, mice with gene deletion of matri

248 We report that apoptosis occurs in a human vascular calcification model in which postconfluent vasc

249 Osteopontin, however, appears to block vascular calcification most likely by preventing calcium

250 In chronic kidney disease (CKD) vascular calcification occurs in response to deranged ca

251 Vascular calcification often occurs with advancing age,

252 tomographic (CT) images were used to overlay vascular calcification on FE MR angiographic images as c

253 Of the known circulating regulators of vascular calcification (OPN, osteoprotegerin, and leptin

254 To examine the role of OPN in vascular calcification, OPN mutant mice were crossed wit

255 growth factor 23 levels but had no effect on vascular calcification or osteodystrophy.

256 Vascular calcification paralleled enhanced aortic osteoc

257 The results indicate that vascular calcification persists after reversal of uremia

258 Vascular calcification powerfully predicts mortality and

259 Vascular calcification predicts an increased risk for ca

260 ormation, and their localization at sites of vascular calcification raises the question of their role

261 crease in femoral neck bone mineral density; vascular calcification remained unchanged in both groups

262 osphate concentration, bone mineral density, vascular calcification, renal function, patient and graf

263 In chronic kidney disease, vascular calcification, renal osteodystrophy, and phosph

264 implicated in the induction or inhibition of vascular calcification, respectively.

265 e to protect skeletal health with respect to vascular calcification risk.

266 of mineral metabolism in ESRD may influence vascular calcification risk.

267 Vascular calcification scores were retrospectively assig

268 se mechanisms creates the "perfect storm" of vascular calcification seen in ESRD.

269 dentified as an important contributor to the vascular calcification seen in patients with chronic kid

270 3(-/-)/klotho(-/-) mice show soft tissue and vascular calcification, severe muscle wasting, hypogonad

271 Recent studies have suggested that vascular calcification shares several features with skel

272 ratide, a PTH1R agonist that inhibits murine vascular calcification, suppressed vascular BMP2-Msx2-Wn

273 In a rat model of CKD and vascular calcification, tenapanor reduced sodium and pho

274 aracterized by excessive atherosclerosis and vascular calcification that leads to premature death, pr

275 lium is a source of osteoprogenitor cells in vascular calcification that occurs in disorders with hig

276 of the correlation of hyperphosphatemia and vascular calcification, the ability of extracellular ino

277 parasitic infections, pulmonary amyloidosis, vascular calcification, the idiopathic disorder pulmonar

278 the combined use of inhibitors that work on vascular calcification through distinct molecular mechan

279 trate that androgens play a role in inducing vascular calcification through the AR.

280 enic protein (BMP)-2, a proposed mediator of vascular calcification through up-regulation of the oste

281 fer a novel explanation of the phenomenon of vascular calcification under hyperphosphatemic condition

282 ults were obtained in two in vitro models of vascular calcification (uremic serum and high-calcium an

283 Vascular calcification (VC) is often associated with car

284 odel of chronic kidney disease (CKD)-induced vascular calcification (VC) that complicates the metabol

285 ets, a model of the metabolic syndrome, have vascular calcification (VC) worsened by chronic kidney d

286 y are characterized by hyperphosphatemia and vascular calcification (VC).

287 Vascular calcifications (VCs) are a cardiovascular risk

288 e results suggest that M/Ms enhance in vitro vascular calcification via 2 independent mechanisms: cel

289 lance as seen in patients with ESRD promotes vascular calcification via multiple mechanisms and may e

290 High doses induce vascular calcification; vitamin D3 deficiency, however,

291 The beneficial effect of Klotho on vascular calcification was a result of more than its eff

292 The effect of MGP mutagenesis on vascular calcification was determined in calcifying vasc

293 To evaluate its possible role in vascular calcification, we assessed its in vitro effects

294 To evaluate BMP2-Msx2 signaling in vascular calcification, we studied primary aortic myofib

295 acic and pericardial fat are associated with vascular calcification, which suggests that these fat de

296 hibited increased aortic O-GlcNAcylation and vascular calcification, which was also associated with i

297 ogical evidence has shown the coexistence of vascular calcification with both atherosclerosis and ost

298 gnificant differences between progression of vascular calcification with dalcetrapib compared to that

299 both SCD1 and SCD2 in SMCs displayed severe vascular calcification with increased ER stress.

300 hese data demonstrate a novel association of vascular calcification with smooth muscle cell phenotypi