ライフサイエンスコーパス: iron overload

1 present in vivo, e.g., under conditions of "iron overload".

2 urden generalizes to other human diseases of iron overload.

3 and serum hepcidin levels leading to severe iron overload.

4 nsfusion requirements resulting in secondary iron overload.

5 ing or treating the toxicity associated with iron overload.

6 and patients incur incremental transfusional iron overload.

7 opoiesis on hepcidin may also play a role in iron overload.

8 ecretion and prevented recurrence of hepatic iron overload.

9 olic dysfunction, and only rarely myocardial iron overload.

10 th or causes diseases, including anaemia and iron overload.

11 e intravenous deferoxamine to treat systemic iron overload.

12 as only 1 patient had evidence of myocardial iron overload.

13 erabsorption of iron is the leading cause of iron overload.

14 n (NTBI), which appears in the plasma during iron overload.

15 influences from erythropoiesis, anemia, and iron overload.

16 decreased hepcidin production, and secondary iron overload.

17 observed and can significantly contribute to iron overload.

18 rs during mild oxidative stress triggered by iron overload.

19 causing ferritin synthesis in the absence of iron overload.

20 ic (Trf(hpx/hpx) ) mice that develop hepatic iron overload.

21 ions, such as hereditary hemochromatosis and iron overload.

22 gene has a well documented association with iron overload.

23 lebotomy) for children with SCA, stroke, and iron overload.

24 d can still develop serious complications of iron overload.

25 ed with excitotoxicity, but also in those of iron overload.

26 ferroportin (Fpn), resulting in parenchymal iron overload.

27 chelator for the treatment of transfusional iron overload.

28 oral chelator, in adults with transfusional iron overload.

29 es but have associated morbidities including iron overload.

30 on and transfusion therapy contribute to the iron overload.

31 way to manage children with SCA, stroke, and iron overload.

32 d absorption of dietary iron, and eventually iron overload.

33 opoiesis and iron dysregulation resulting in iron overload.

34 enic, and hemochromatosis is associated with iron overload.

35 that appears in the plasma during pathologic iron overload.

36 to unchecked iron absorption and subsequent iron overload.

37 ed to controls (P = 0.02), likely related to iron overload.

38 such patients might be therapeutic, limiting iron overload.

39 risk phenotype associated with all forms of iron overload.

40 ntestinal iron absorption that may result in iron overload.

41 centrations that correlated with severity of iron overload.

42 n, were observed together with mitochondrial iron overload.

43 d the ineffective erythropoiesis, but led to iron overload.

44 cidate the associated molecular mechanism of iron overload.

45 with reduced hepcidin expression and tissue iron overload.

46 iac-specific deletion leads to fatal cardiac iron overload.

47 netic disorders characterized by parenchymal iron overload.

48 ored red blood cells) and primary (Hfe(-/-)) iron overload.

49 usceptibility to mild-to-moderate late-onset iron overload.

50 emia major and is associated with myocardial iron overload.

51 ere negative for viral hepatitis B and C and iron overload.

52 the relationship between ECV and myocardial iron overload.

53 ates ineffective erythropoiesis, anemia, and iron overload.

54 l effect of the iron chelator deferiprone on iron overload.

55 sis, many patients have unexplained signs of iron overload.

56 tations in BMP6 in patients with unexplained iron overload.

57 band was noted to have dyserythropoiesis and iron overload.

58 mice, restores hepcidin levels and corrects iron overload.

59 ssive absorption of dietary iron, leading to iron overload.

60 rried out in a family with A1ATD and hepatic iron overload.

61 uction is required, regardless of myocardial iron overload.

62 cidin levels indicate a significant risk for iron overload.

63 mary use of chelation has been transfusional iron overload.

64 that suppresses hepcidin expression despite iron overloading.

65 /g liver phantom) to 5 mg Fe/g liver phantom iron overload (100X overdose).

66 neral density [BMD], 23.2%), serum ferritin (iron overload, 24.0%), and pulmonary function testing/ch

67 oad had higher ECV than did patients without iron overload (31.3% +/- 2.8 vs 28.2% +/- 3.4, P = .030)

68 lu) in 6 unrelated patients with unexplained iron overload (9% of our cohort).

69 Iron deficiency and iron overload affect over a billion people worldwide.

70 lation should be considered in patients with iron overload and a history of GBCA exposure.

71 te that additional novel tools for measuring iron overload and a molecular-mechanism-driven descripti

72 These data showed high sensitivity to iron overload and a strong relationship between quantita

73 t study to determine the association between iron overload and adult allogeneic hematopoietic cell tr

74 Here we investigated the effects of iron overload and age on cardiac hypertrophy using 1-, 5

75 e found no association between pretransplant iron overload and allogeneic HCT outcomes.

76 To better understand the tissue iron overload and anemia previously reported in a human

77 rform the chronic phlebotomies to reduce the iron overload and clear the dermatologic lesions in porp

78 o difference in ECV between patients without iron overload and control subjects (P = .647).

79 iron homeostasis, causing both mitochondrial iron overload and cytosolic iron deficiency.

80 Iron overload and deficiency can adversely affect human

81 tive disorder characterized by mitochondrial iron overload and disruption in Fe-S cluster synthesis.

82 In addition, preventing iron overload and formation of reactive oxygen species m

83 Transfusional iron overload and gonadal failure are addressed, followe

84 ia in mice with either genetic or iatrogenic iron overload and in human plasma.

85 Conversely, organismal iron overload and increased adipocyte ferroportin expres

86 itions, hamp1 was upregulated in response to iron overload and infection and downregulated during ane

87 dent thalassemia (NTDT) patients may develop iron overload and its associated complications despite r

88 is effectively protected from the peripheral iron overload and maintains normal iron content.

89 In HJV-null (Hjv(-/-)) mice that have severe iron overload and marked suppression of hepcidin express

90 he iron distribution throughout the heart in iron overload and provide calibration in humans for card

91 cause of hyperferritinemia in the absence of iron overload and provides a possible diagnostic schema.

92 uced production of erythrocytes, anemia, and iron overload and PV by erythrocytosis and thrombosis.

93 expression under conditions of simultaneous iron overload and stress erythropoiesis, and impairing t

94 sociations for fatty liver disease and liver iron overload and their prevalence in a large-scale popu

95 nducing hepcidin expression in patients with iron overload and/or chronic liver diseases.

96 enesis of primary hemochromatosis, secondary iron overload, and anemia of inflammatory disease.

97 examined in 20 HFE-HH males with significant iron overload, and compared to seven male HFE wild-type

98 es including fibrosis, cirrhosis, steatosis, iron overload, and hepatocellular carcinoma.

99 t mice have severe microcytic anemia, tissue iron overload, and hepcidin deficiency.

100 munosuppression, anatomic barrier breakdown, iron overload, and hyperglycemia/acidosis.

101 growth phenotype, reversed the mitochondrial iron overload, and increased aconitase activity.

102 taneous leg ulceration, renal insufficiency, iron overload, and liver dysfunction.

103 han in prior studies, the high penetrance of iron overload, and the frequency of at-risk genotypes, i

104 protects against tissue iron accumulation in iron overload anemias.

105 autosomal dominant disease with parenchymal iron overload, apparently due to the resistance of mutan

106 A in circulating blood cells, and markers of iron overload are associated with high PlGF and early mo

107 Chronic anemia and iron overload are believed to lie behind these abnormali

108 Hemochromatosis is a disorder of iron overload arising mostly from mutations in HFE.

109 The complications of iron overload, arising from transfusions that represent

110 Iron overload as a result of blood transfusions and exce

111 correlated to hepatic T2* times (ie, hepatic iron overload because of frequent blood transfusions; P<

112 deposition occurs in pediatric patients with iron overload but normal renal and hepatic function who

113 rine beta-thalassemia not only mitigates the iron overload, but also the severity of the anemia.

114 best known as being associated with cellular iron overload, but the mechanism by which HFE H63D might

115 In this study, the impact of iron overload by SPIONs was assessed on a mouse cirrhosi

116 Iron overload can increase cellular oxidative stress lev

117 accumulating excessive iron in body organs (iron overload) can damage or even destroy an organ.

118 Using adiponectin for adjuvant therapies in iron-overload cardiac dysfunction may be an option in th

119 The prevalence of iron overload cardiomyopathy (IOC) is increasing.

120 ortantly these changes preceded the onset of iron overload cardiomyopathy, providing an early biomark

121 ated with iron dextran for 4 weeks to induce iron-overload cardiomyopathy.

122 Cardiac iron overload causes most deaths in beta-thalassemia maj

123 ively reduce cellular ferritin expression in iron overloaded cells and regulate intracellular iron le

124 Iron-overloaded cells harboring a constitutively active

125 the suppression of hepcidin and the systemic iron overload characteristic of this disease.

126 Fpn C326S mice had systemic iron overload compared to wild type and had the fastest

127 Patients with iron overload completed 1.5T R2*-MRI examination and liv

128 acute-phase response and the consequences of iron overload conditions on susceptibility to bacterial

129 loading in TM are directly relevant to other iron-overload conditions, including in particular Diamon

130 the patients showed a significant myocardial iron overload correlated with lower compliance to chelat

131 -null mouse) and in two nongenetic models of iron overload (cytomegalovirus infection and treatment w

132 Iron overload damages many organs.

133 of hepcidin in beta-thalassemic mice limits iron overload, decreases formation of insoluble membrane

134 neteen patients (63.3%) had prior myocardial iron overload (defined as midseptal T2* < 20 msec on any

135 Mice with a mosaic pattern of RPE-specific iron overload demonstrated co-localization of iron-induc

136 Because iron overload develops in some MDS patients who do not r

137 gside rapid decreases in LIC in this heavily iron-overloaded, difficult-to-treat population.

138 als as an iron chelator for the treatment of iron overload disease because of its nephrotoxicity.

139 Hereditary hemochromatosis, an iron overload disease caused by a deficiency in the iron

140 e dominant inheritance of hepcidin resistant iron overload disease.

141 chelator currently used for the treatment of iron-overload disease and has been implemented as an alt

142 epithelium (RPE) and their regulation in the iron-overload disease hemochromatosis were examined.

143 rapeutics isa practical approach to treating iron overload diseases associated with diminished hepcid

144 active iron chelators to treat transfusional iron-overload diseases, e.g., thalassemia, is overviewed

145 hemochromatosis (JH), a rapidly progressive iron overload disorder in which expression of hepcidin,

146 The most common inherited iron overload disorder results from defects in the HFE g

147 y hemochromatosis (HH) is a common inherited iron overload disorder.

148 ons cause juvenile hemochromatosis, a severe iron overload disorder.

149 ions in HFE are the most common cause of the iron-overload disorder hereditary hemochromatosis.

150 epcidin-ferroportin axis are a main cause of iron overload disorders but can also cause iron-restrict

151 es that minihepcidins could be beneficial in iron overload disorders either used alone for prevention

152 ysiology of many of the genetically distinct iron overload disorders, collectively termed hereditary

153 te disease severity in mouse models of human iron overload disorders.

154 broadly effective treatments for hereditary iron overload disorders.

155 hepcidins may be useful for the treatment of iron overload disorders.

156 clinically to remove iron from patients with iron overload disorders.

157 cause of tissue-iron accumulation in anemic iron-overload disorders caused by hemolytic anemia.

158 a novel therapeutic target in several anemic iron-overload disorders.

159 is and chronic anemia and is associated with iron overload due to both transfused iron and increased

160 n and alpha-syn in exosomes, suggesting that iron overload due to impaired ferritinophagy or other ca

161 in human hemochromatosis protein (HFE) cause iron overload due to reduced hepatic hepcidin secretion.

162 mice developed microcytic anemia and tissue iron overload, especially in the spleen.

163 ction of anemia, alloimmunization, and organ iron overload (for which the role of iron chelation rema

164 he presence of iron deficiency and secondary iron overload from thalassemia.

165 multiparametric CMR assessment of myocardial iron overload, function, and fibrosis in a cohort of ped

166 Median LIC in the iron-overload group was 4.3 mg/g (range, 1.9-25.4).

167 to hepcidin knockout mice with pre-existing iron overload had a more moderate effect and caused part

168 xteen of twenty-two participants with severe iron overload had glyceronephosphate O-acyltransferase (

169 Patients with prior myocardial iron overload had higher ECV than did patients without i

170 Humans with aceruloplasminemia causing RPE iron overload had increased RPE C3d deposition.

171 Moreover, thalassemic mice with established iron overload had significant improvement in tissue-iron

172 Brain iron overload has a detrimental role in brain injury aft

173 to experience deleterious cardiac effects of iron overload has been the major argument in favor of ir

174 age-dependent cardiac stress exacerbated by iron overload hemochromatosis.

175 Nevertheless, TFR2 mutations cause iron overload (hemochromatosis type 3) without overt ery

176 at mice and humans with a form of hereditary iron overload, hemochromatosis, exhibit loss of beta-cel

177 Mutations in ferroportin cause a form of the iron overload hereditary disease hemochromatosis.

178 Our study indicates that preventing iron overload improves beta-thalassemia and strengthens

179 vel SLC40A1 mutation p.R489K segregated with iron overload in a family with clinical and histopatholo

180 erythropoiesis, corrected anemia and limited iron overload in a mouse model of beta-thalassemia inter

181 ates hepcidin suppression and contributes to iron overload in a mouse model of beta-thalassemia.

182 eficiency (A1ATD) is associated with hepatic iron overload in a subgroup of patients.

183 ssential for osteoclast differentiation, and iron overload in a variety of hematologic diseases is as

184 lementation with 2,5-DHBA alleviates splenic iron overload in bdh2 null mice.

185 2alpha signaling is critical for progressive iron overload in beta-thalassemia and may be a novel the

186 10muM) pretreatment abrogates the effects of iron overload in brain endothelial cells protecting cell

187 tment to prevent recurrent stroke and manage iron overload in children chronically transfused over 7

188 ed to embryonic lethality potentially due to iron overload in developing embryos.

189 nding is interesting in light of the role of iron overload in diabetes.

190 chanism, A1ATD could be a trigger of hepatic iron overload in genetically predisposed individuals or

191 epcidins for the prevention and treatment of iron overload in hepcidin-deficient mice.

192 Iron overload in hereditary hemochromatosis and beta-tha

193 Hepcidin deficiency results in iron overload in hereditary hemochromatosis and ineffect

194 he iron exporter ferroportin (Fpn) result in iron overload in macrophages or hepatocytes depending up

195 partially result from its ability to prevent iron overload in macrophages.

196 nguinity, highlighting the increased risk of iron overload in many countries of the developing world

197 This is the first study to demonstrate that iron overload in mice results in increased bone resorpti

198 tes to pathological hepcidin suppression and iron overload in mice with nontransfused beta-thalassemi

199 cific deletion of either Alk2 or Alk3 causes iron overload in mice.

200 icient hepcidin synthesis is responsible for iron overload in minimally transfused patients with this

201 s that have been previously shown to prevent iron overload in murine models of hemochromatosis and in

202 and its tissue distribution, is the cause of iron overload in nearly all forms of hereditary hemochro

203 ation with deferasirox significantly reduces iron overload in NTDT patients with a frequency of overa

204 e(hi) iron handling coincides with adipocyte iron overload in obese mice.

205 Deferasirox was shown to reduce iron overload in patients with hemochromatosis and may b

206 transfusions are one of the major causes of iron overload in several of these disorders, including b

207 p2(fl/fl) (Bmp2(LSECKO)) mice caused massive iron overload in the liver and increased serum iron leve

208 ce of abnormal sideroblasts characterized by iron overload in the mitochondria, called RS.

209 Central to early identification of cardiac iron overload in TM is the estimation of cardiac iron by

210 chelation strategies would reduce myocardial iron overload in TM patients compared with placebo.

211 The most common complications are iron overload in transfused patients and syndrome-specif

212 he key iron regulator hepcidin (HAMP) causes iron overload in untransfused patients affected by beta-

213 mRNA levels are increased in mouse models of iron overload, indicating that TGF-beta1 may contribute

214 te hepatic porphyrias, identification of the iron overload-induced inhibitor of hepatic uroporphyrin

215 dative stress and protected DKO mice against iron overload-induced retinal degeneration.

216 in this population should use LIC to define iron overload instead of ferritin.

217 prevalence of fatty liver diseases and liver iron overload is 42.2% (1082 of 2561) and 17.4% (447 of

218 A strong recommendation to assess iron overload is accompanied by a moderate strength reco

219 Iron overload is associated with increased diabetes risk

220 Iron overload is associated with low levels of hepcidin,

221 Iron overload is the hallmark of hereditary hemochromato

222 Cardiac damage associated with iron overload is the most common cause of morbidity and

223 is associated with cognitive impairment, yet iron overload is thought to promote neurodegenerative di

224 sfusions, a consequence of which is systemic iron overload leading to acute heart failure.

225 ere defined as no iron overload (N = 28) and iron overload (LIC >1.8 mg/g; N = 60).

226 Livers of neogenin mutant mice exhibit iron overload, low levels of hepcidin, and reduced BMP s

227 itary liver diseases resulting in copper and iron overload may cause significant morbidity and mortal

228 An iron overload may induce pancreatic islet damage and inc

229 ies, which are increased under conditions of iron overload, may also hamper erythropoiesis.

230 Patients were severely iron overloaded: mean liver iron concentration (LIC) 20.

231 s detected in the visceral adipose tissue of iron overloaded mice, and gene expression analysis of vi

232 In addition, it removes iron from iron overloaded mice, including models of acquired (iron

233 In addition, AAV-ADIPOQ-treated iron-overload mice had lower expression of inflammatory

234 RPE cells from iron-overloaded mice exhibit several features of tumor c

235 Compared with the placebo group, iron-overloaded mice exhibited dose-dependent increased

236 Iron-overloaded mice had increased reactive oxygen speci

237 and intercellular adhesion molecule-1, than iron-overloaded mice not treated with AAV-ADIPOQ.

238 Treatment of iron-overloaded mice with the antioxidant N-acetyl-L-cys

239 deposition and restored cardiac function in iron-overloaded mice.

240 fect of iron excess in bone, we generated an iron-overloaded mouse by injecting iron dextran at 2 dos

241 Patients were defined as no iron overload (N = 28) and iron overload (LIC >1.8 mg/g;

242 ed the efficacy and safety of deferasirox in iron-overloaded NTDT patients.

243 it of Fe-S cluster enzymes and mitochondrial iron overload occur in the myocardium of individuals wit

244 in to neutralize circulating hemoglobin, and iron overload occurred in kidney proximal tubules, which

245 Hamp2 did not respond to either iron overload or anemia but was highly upregulated durin

246 t in mouse models of these diseases prevents iron overload or decreases its potential toxicity, natur

247 utic target for the treatment of diseases of iron overload or deficiency.

248 erum of AN patients, without any evidence of iron overload or inflammation.

249 assemia may correlate to the disease itself, iron overload or the chelating agents used.

250 anemias, GDF15 expression may contribute to iron overloading or other features of the disease phenot

251 the most significant association with severe iron overload (P = 3 x 10(-6) ; P = 0.033 by the likelih

252 as the best threshold for predicting cardiac iron overload (P=0.001 and P<0.0001, respectively).

253 ecific KO mice fully recapitulate the severe iron overload phenotype observed in the total KO mice, w

254 The iron overload phenotype was more marked in Alk3- than in

255 Recent data suggest that markers of iron overload portend a relatively poor prognosis, and r

256 the hereditary hemochromatosis, resulting in iron overload predominantly in the liver.

257 cardiac isoprostane levels, suggesting that iron overload promotes oxidative stress and cardiac hype

258 In mice, systemic iron overload protected against renal ischemia-reperfusi

259 Measuring resulting iron overload remains a challenge.

260 The cause of the systemic iron overload remains to be discovered.

261 of the most consistent findings in advanced iron overload resulting from hemochromatosis.

262 eta-thalassemia develop progressive systemic iron overload, resulting in high morbidity and mortality

263 The Hemochromatosis and Iron Overload Screening (HEIRS) Study screened 99,711 pr

264 The Hemochromatosis and Iron Overload Screening (HEIRS) Study was a multicenter

265 polymorphisms associated with variability of iron overload severity in HFE-associated hemochromatosis

266 eased hepatic Bmp6 mRNA levels, and systemic iron overload similar to mice deficient for Hjv alone.

267 gated disease complications of IE, including iron overload, splenomegaly, and bone pathology, while r

268 of these gene expression changes favored an iron-overloaded state.

269 ntify disease severity related to myocardial iron overload states or glycosphingolipid accumulation i

270 In multivariate analyses, iron-overload status did not impact risks of overall mor

271 ials for stroke prevention were examined for iron overload (STOP and STOP2; n = 271).

272 equent problem in disorders characterized by iron overload, such as the thalassemias and hereditary h

273 al cellular iron content under conditions of iron overload, suggesting that the stm3944-encoded prote

274 Dysmetabolic iron overload syndrome (DIOS) is a common cause of hyper

275 on, we characterized a model of dysmetabolic iron overload syndrome in which an iron-enriched diet in

276 is a potential drug target for patients with iron overload syndromes because its levels are inappropr

277 equently be developed into new therapies for iron overload syndromes.

278 ntly lower in patients with prior myocardial iron overload than in control subjects (850.3 +/- 115.1

279 es a quantitative understanding of the liver iron overload that arises in this disease.

280 In all cases of iron overload, the expression of FLVCR and PCFT was upre

281 ry hemochromatosis, mutations in HFE lead to iron overload through abnormally low levels of hepcidin.

282 vival in MDS, direct evidence linking tissue iron overload to poor survival or in particular to cardi

283 ning for stroke risk, improved management of iron overload using oral chelators and non-invasive MRI

284 imary care participants in North America for iron overload using serum ferritin and transferrin satur

285 Magnetic resonance imaging showed that iron overload was absent in nine patients, mild in one p

286 eferasirox in reducing or preventing cardiac iron overload was assessed in 192 patients with beta-tha

287 A homogeneous pattern of myocardial iron overload was associated with a negative cardiac rem

288 Prevalence of fatty liver diseases and iron overload was calculated (weighted by probability of

289 Iron overload was mediated by decreased hepatic expressi

290 Iron overload was observed in 17.4% (447 of 2561 partici

291 The regulation of heme transporters by iron overload was studied in two genetic models of hemoc

292 Myocardial and liver iron overload were measured by T2* multiecho technique.

293 of Tmprss6 in Hfe(-/-) mice reduced systemic iron overload, whereas homozygous loss caused systemic i

294 90% transferrin saturation and massive liver iron overload, whereas Smad1(fl/fl);Smad5(fl/wt);Cre(+)

295 patients affected by these disorders exhibit iron overload, which is the main cause of morbidity and

296 Observed familial clustering of hepatic iron overload with A1ATD suggests a genetic cause, but g

297 inct congenital disorders can lead to tissue-iron overload with anemia.

298 d elevations in iron absorption, which cause iron overload with associated organ toxicities.

299 both Hfe and Tfr2 caused more severe hepatic iron overload with more advanced lipid peroxidation, inf

300 ble iron chelators is summarized for cardiac iron overload without overt cardiac dysfunction.