ライフサイエンスコーパス: vascular calcification

1 actor for proteins involved in prevention of vascular calcification.

2 osteodystrophy, and prevented CKD-stimulated vascular calcification.

3 esigning methods to improve defenses against vascular calcification.

4 be potential therapies for the treatment of vascular calcification.

5 m to contribute osteoprogenitor cells to the vascular calcification.

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

7 animals had an impaired capacity to inhibit vascular calcification.

8 uction, and AAA formation without disturbing vascular calcification.

9 encing coronary heart disease and attenuates vascular calcification.

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

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

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

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

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

15 d protection from factors known to stimulate vascular calcification.

16 to the mechanisms underlying atherosclerotic vascular calcification.

17 ) plays an important role in atherosclerotic vascular calcification.

18 rophosphate, another endogenous inhibitor of vascular calcification.

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

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

21 tors of mineral metabolism and inhibitors of vascular calcification.

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

23 est that osteoprotegerin may protect against vascular calcification.

24 chondrogenic" profile has been implicated in vascular calcification.

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

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

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

28 icalcitol may protect against CKD-stimulated vascular calcification.

29 crease risk and complicate the management of vascular calcification.

30 rphosphatemia is an important contributor to vascular calcification.

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

32 ence suggests that they could participate in vascular calcification.

33 ences of prolonged glucocorticoid therapy on vascular calcification.

34 unknown role for HDAC9 in the development of vascular calcification.

35 y program is upregulated in association with vascular calcification.

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

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

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

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

40 rocess thought critical in the initiation of vascular calcification.

41 between MMP-mediated elastin degradation and vascular calcification.

42 h early success in preventing progression of vascular calcification.

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

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

45 emia and have been associated with increased vascular calcification.

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

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

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

49 entiation and bone formation are involved in vascular calcification.

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

51 Relatively little is known about noncoronary vascular calcification.

52 is that exogenous androgen treatment induces vascular calcification.

53 Dalcetrapib therapy did not affect vascular calcification.

54 levant therapeutic targets for mitigation of vascular calcification.

55 injury dramatically reduced the severity of vascular calcification.

56 es including restenosis, atherosclerosis and vascular calcification.

57 new therapeutic targets in the management of vascular calcification.

58 ascular diseases such as atherosclerosis and vascular calcification.

59 new approaches to developing treatments for vascular calcification.

60 8:0-PA) mediate SFA-induced lipotoxicity and vascular calcification.

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

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

63 ascular diseases such as atherosclerosis and vascular calcification.

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

65 key lipogenic pathway in SMCs that mediates vascular calcification.

66 characteristic events in the development of vascular calcification.

67 osphorylation and activation, thus promoting vascular calcification.

68 egenerative cardiovascular disease including vascular calcification.

69 celerated aging that includes osteopenia and vascular calcifications.

70 ic inflammation, endothelial dysfunction and vascular calcifications.

71 Vascular calcification, a pathologic response to defecti

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

73 Vascular calcification, a risk factor for cardiovascular

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

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

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

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

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

79 Effects of phosphate-lowering medication on vascular calcification and arterial stiffness in CKD rem

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

81 are instrumental in vascular disease such as vascular calcification and atherosclerosis.

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

83 sphotoxicity, including excessive Pi-related vascular calcification and chronic tissue injury.

84 tein (BMP)-4, which plays a key role in both vascular calcification and endothelial barrier damage ob

85 with ATP, levamisole, and ARL67156 prevented vascular calcification and extended longevity by 12% in

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

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

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

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

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

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

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

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

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

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

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

97 nanoparticles delivered EDTA at the site of vascular calcification and reversed mineral deposits wit

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

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

100 lls on smooth muscle cell mineralization and vascular calcification and the possible mechanisms invol

101 ned how VSMC phenotypic switching influences vascular calcification and the possible role of the uniq

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

103 Vascular calcification and vascular metabolic activity r

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

119 5-dihydroxyvitamin D3 [1,25(OH)(2)D] levels; vascular calcifications; and early death.

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

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

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

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

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

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

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

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

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

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

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

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

132 Klotho ameliorates vascular calcification by enhancing phosphaturia, preser

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

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

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

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

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

138 Vascular calcification contributes to the high risk of c

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

140 Vascular calcification develops within atherosclerotic l

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

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

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

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

145 osphate deficiency may explain the excessive vascular calcification found in children with Hutchinson

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

147 module (ie, the "calcificasome") by mapping vascular calcification genes (proteins) to the human vas

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

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

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

151 ce for a role of these toxins in CKD-related vascular calcification has not been reported.

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

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

154 Hyperphosphatemia and vascular calcification have emerged as cardiovascular ri

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

156 Vascular calcification impairs vessel compliance and inc

157 7 ameliorates chronic kidney disease induced-vascular calcification in 5/6 nephrectomized ApoE(-/-) m

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

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

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

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

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

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

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

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

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

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

168 of SIRT1 may be responsible for perpetuating vascular calcification in diabetes.

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

170 Treatment with ATP prevented vascular calcification in HGPS mice but did not extend l

171 investigate mechanisms that cause excessive vascular calcification in HGPS.

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

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

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

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

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

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

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

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

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

181 plementation, compared to placebo, decreases vascular calcification in people with type 2 diabetes an

182 Treatment with pyrophosphate inhibited vascular calcification in progeroid mice.

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

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

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

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

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

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

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

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

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

195 e to endothelial-mesenchymal transitions and vascular calcification, including bone morphogenetic pro

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 is a common complication in ather

203 Vascular calcification is a common complication in CKD,

204 Vascular calcification is a common feature of major card

205 Vascular calcification is a common problem among the eld

206 Vascular calcification is a complex biological process t

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

208 Vascular calcification is a frequent cause of morbidity

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

210 Vascular calcification is a highly regulated process inv

211 Vascular calcification is a highly regulated process tha

212 Vascular calcification is a major contributor to cardiov

213 Vascular calcification is a major contributor to the pro

214 Vascular calcification is a major risk factor for cardio

215 Vascular calcification is a predictor of cardiovascular

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

217 Vascular calcification is a regulated process that invol

218 Vascular calcification is a serious cardiovascular compl

219 Widespread vascular calcification is a ubiquitous feature of aging

220 Vascular calcification is an active cell-mediated proces

221 Vascular calcification is associated with an increased r

222 Vascular calcification is associated with cardiovascular

223 Vascular calcification is associated with significant mo

224 Vascular calcification is common in chronic kidney disea

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

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

227 Vascular calcification is highly associated with cardiov

228 Vascular calcification is highly correlated with cardiov

229 Vascular calcification is known to be a risk factor for

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

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

232 Vascular calcification is present in many pathological c

233 Vascular calcification is prevalent in aging as well as

234 Vascular calcification is prevalent in the aging populat

235 Vascular calcification is recognized as an independent p

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

237 Vascular calcification is strongly linked with increased

238 However, the effect of vitamin K on vascular calcification is unknown.

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

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

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

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

243 n K supplementation on vascular stiffness or vascular calcification measures.

244 ome (myocardial structure/function, fitness, vascular calcification), mechanisms, and outcomes over 2

245 Gla protein-deficient mice, a model of human vascular calcification, mice lacking HDAC9 had a 40% red

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

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

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

249 Vascular calcification often occurs with advancing age,

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

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

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

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

254 Vascular calcification paralleled enhanced aortic osteoc

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

256 Vascular calcification powerfully predicts mortality and

257 Vascular calcification predicts an increased risk for ca

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

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

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

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

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

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

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

265 Vascular calcification scores were retrospectively assig

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

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

268 3(-/-)/klotho(-/-) mice show soft tissue and vascular calcification, severe muscle wasting, hypogonad

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

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

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

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

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

274 Vascular calcification, the formation of calcium phospha

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

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

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

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

279 Finally, in Klotho(-/-) mice with marked vascular calcification, treatment with spironolactone al

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

281 phosphatemia-induced inflammation aggravates vascular calcification (VC) by increasing vascular smoot

282 ncriminated as probable cause of accelerated vascular calcification (VC) in patients on hemodialysis.

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 (IP6) is a natural product known to inhibit vascular calcification (VC), but with limited potency an

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

288 Vascular calcifications (VCs) are a cardiovascular risk

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

290 In CKD, both IS and PCS directly promote vascular calcification via activation of inflammation an

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

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

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

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

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

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

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

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

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

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