ライフサイエンスコーパス: nephron

1 brotic agent TGF-beta by this portion of the nephron.

2 s in the trilaminar filtration layers of the nephron.

3 on in glomerulus, and in proximal and distal nephron.

4 ong the proximo-distal axis of the mammalian nephron.

5 shed into the urine by the cells lining the nephron.

6 limb and in the aldosterone-sensitive distal nephron.

7 rturbations that develop in this part of the nephron.

8 tion of Na(+) transport in the distal kidney nephron.

9 es a prostaglandin transporter in the distal nephron.

10 ical membrane-determining CRB complex in the nephron.

11 dimorphic pattern of transporters along the nephron.

12 ate into the various tubular segments of the nephron.

13 ial for proper sodium handling in the distal nephron.

14 verse group of malignancies arising from the nephron.

15 ug exposure relative to solubility along the nephron.

16 nd lef1-expressing progenitor cells form new nephrons.

17 UMOD protein, which is normally secreted by nephrons.

18 hron GFR assesses the function of individual nephrons.

19 rotic glomeruli and hypertrophy of remaining nephrons.

20 on endowment at birth and subsequent loss of nephrons.

21 to a smaller NPC pool and formation of fewer nephrons.

22 trophy in tubule segments along the affected nephrons.

23 Distal nephron acid secretion is mediated by highly specialized

24 Although the kidney cannot generate new nephrons after birth, suggesting a low level of regenera

25 e morphology and reduced regeneration of new nephrons after injury.

26 New nephron aggregates are patterned by Wnt signaling, with

27 NAs exhibit segmental distribution along the nephron and CDs.

28 intenance of Aqp2-expressing cells in distal nephron and collecting duct segments in adult kidneys.

29 onally related cell types are specified from nephron and collecting system progenitor populations.

30 re released from all regions of the kidney's nephron and from other cells that line the urinary tract

31 nd aquaporins at various positions along the nephron and in the outer and inner medulla.

32 s the glomerular filtrate passes through the nephron and into the renal medulla, electrolytes, water,

33 for Na(+) reabsorption in the distal kidney nephron and is regulated by numerous hormones, including

34 Thus, the lineage boundary between the nephron and renal interstitial compartments is maintaine

35 y, indicating a lineage boundary between the nephron and renal interstitial compartments.

36 differentiated human cells in an appropriate nephron and stromal context.

37 define sexual dimorphic phenotypes along the nephron and suggest that lower proximal reabsorption in

38 e transcriptional distinction between distal nephron and ureteric epithelium in human fetal kidney, w

39 PCs) give rise to all segments of functional nephrons and are of great interest due to their potentia

40 After a radical nephrectomy, larger nephrons and nephrosclerosis predicted progressive CKD,

41 ofenac's uptake potential, effects on kidney nephrons and relatively small safety margin for some sur

42 s contribute exclusively to the main body of nephrons and renal interstitial tissues, respectively, i

43 ignatures lays the foundation for rebuilding nephrons and uncovering the pathogenesis of kidney disor

44 progenitors, podocytes, proximal and distal nephron, and ureteric epithelium.

45 clerosis, podocyte density in juxtamedullary nephrons, and filtration slit density.

46 te density in superficial and juxtamedullary nephrons, and podocyte filtration slit density.

47 tion rate (GFR) assesses the function of all nephrons, and the single-nephron GFR assesses the functi

48 ains of cell proliferation in the elongating nephron; and tubule fusion where the new nephron plumbs

49 ear the end of gestation, after which no new nephrons are formed.

50 interesting time in development when mature nephrons are present yet nephrogenesis remains extremely

51 ween progenitors of the collecting ducts and nephrons are primarily responsible for kidney developmen

52 ng kidney organoids in mice yield developing nephrons arranged around a symmetrical collecting duct t

53 ignaling in the aldosterone-sensitive distal nephron (ASDN) and inhibition of the potassium-excretory

54 proximal tubule but decreased in the distal nephron because of diminished Na(+) delivery.

55 lculated as the GFR divided by the number of nephrons (calculated as the cortical volume of both kidn

56 petence, the tubular epithelial cells of the nephrons can proliferate to repair the damage after AKI.

57 of ENaC-mediated sodium transport along the nephron cannot be compensated for by other sodium channe

58 ells lacking Pax2 fail to differentiate into nephron cells but can switch fates into renal interstiti

59 kctd15a/b loss primed nephron cells to adopt distal fates by driving slc12a1,

60 cells that express Wnt4, an early marker of nephron commitment, but migrate back into the progenitor

61 The final nephron complement can vary 10-fold, with reduced nephro

62 primarily handled by a short segment of the nephron, comprising part of the distal convoluted tubule

63 al kidney, we show here that, while existing nephron-containing kidney organoids contain distal nephr

64 ed trials of early (ACCORD) and advanced (VA NEPHRON-D) DKD.

65 -fold higher in the advanced DKD population (NEPHRON-D) than in the early DKD population (ACCORD).

66 ncident DKD (ACCORD) and progressive DKD (VA-NEPHRON-D).

67 l outcome from 0.68 (0.02) to 0.75 (0.02) in NEPHRON-D.

68 n hypothesized to predispose to irreversible nephron damage, thereby contributing to initiation and p

69 ly interact in the second part of the distal nephron (DCT2).

70 rine growth restriction is associated with a nephron deficit in humans, and is commonly caused by pla

71 A male-specific 35% nephron deficit in microRNA-210 knockout mice was observ

72 a link between prenatal metabolic stress and nephron deficit via dysregulation of DNA methylation - a

73 istinct organization and cell composition of nephrons dependent on the time of nephron specification,

74 AMP signaling is appropriate in NP and early nephron derivatives, but disappears in mature proximal t

75 1 allele (functionally haploid for Pals1) in nephrons developed a fully penetrant phenotype, characte

76 ere generated to dissect the role of TrkC in nephron development and maintenance.

77 nal stroma, which also essentially modulates nephron development from the metanephric mesenchyme.

78 collecting duct branches radiate and induce nephron development in an arrangement similar to natural

79 molecule(s) regulating FGF signaling during nephron development.

80 tor in ureteric bud branching and subsequent nephron development.

81 eta-catenin signaling, a pathway crucial for nephron differentiation, was misregulated in male kidney

82 , including the aldosterone-sensitive distal nephron, distal colon, and biliary epithelium.

83 nstitutive activation of Notch in developing nephrons does not promote or repress the formation of a

84 In humans and in mice the formation of nephrons during embryonic development reaches completion

85 ith characteristics reflective of both lower nephron endowment at birth and subsequent loss of nephro

86 Low nephron endowment at birth has been associated with an i

87 enewal target assessed as well as for proper nephron endowment in vivo This study suggests that, with

88 Nephron endowment is determined by the self-renewal and

89 tation contribute to the high variability of nephron endowment.

90 enesis, as one potential means of regulating nephron endowment.

91 ewal and differentiation to give rise to all nephron epithelia.

92 contain cells of multiple lineages including nephron epithelial cells.

93 o increase sodium transport in distal kidney nephron epithelial cells.

94 n-containing kidney organoids contain distal nephron epithelium and no ureteric epithelium, this dist

95 The model predicted that the human nephron exhibits glomerulotubular balance, such that pro

96 ade of canonical Wnt signaling inhibited new nephron formation after injury by inhibiting cell prolif

97 ng is required during kidney development for nephron formation and principal cell fate selection with

98 r the first time that PGE2 is a regulator of nephron formation in the zebrafish embryonic kidney, thu

99 In particular, nephron formation, tubular maturation, and the different

100 e number of nephron progenitors and improved nephron formation.

101 ngineered ureteric buds branched and induced nephron formation; when grafted into peri-Wolffian mesen

102 the function of all nephrons, and the single-nephron GFR assesses the function of individual nephrons

103 The single-nephron GFR did not vary significantly according to age

104 How the single-nephron GFR relates to demographic and clinical characte

105 However, single-nephron GFR remains relatively constant with healthy agi

106 00+/-370,000 per kidney, and the mean single-nephron GFR was 80+/-40 nl per minute.

107 A higher single-nephron GFR was associated with a height of more than 19

108 A higher single-nephron GFR was associated with certain risk factors for

109 The mean single-nephron GFR was calculated as the GFR divided by the num

110 mong healthy adult kidney donors, the single-nephron GFR was fairly constant with regard to age, sex,

111 A higher single-nephron GFR was independently associated with larger nep

112 gns of compensation (such as elevated single-nephron GFR) or kidney damage.

113 psy findings were correlated with the single-nephron GFR.

114 ected for age is there an increase in single-nephron GFR.

115 d beta(2) -m excretion with increased single nephron glomerular filtration rate (SNGFR) following uni

116 sorption varies proportionally to the single-nephron glomerular filtration rate.

117 Both are expressed in the late distal nephron; however, no evidence has suggested that these t

118 Nephron hypertrophy and nephrosclerosis may be important

119 C-mediated sodium reabsorption in the distal nephron in the conditions of HS- and hyperglycemia-induc

120 ion tool Osr2Cre removed Hnf4a in developing nephrons in mice, generating a novel model for FRTS.

121 n and gain-of-function studies in developing nephrons in mice.

122 vise strategies to stimulate regeneration of nephrons in situ to restore failing kidney function.

123 or Dermo1-labeled cells were present in the nephron including glomerulus but they were not stained b

124 reduced Na(+) intake, reabsorption along the nephron is adjusted with activation of the renin-angiote

125 The nephron is composed of distinct segments that perform un

126 The nephron is represented as a tubule lined by a layer of e

127 The nephron is the basic physiologic subunit of the mammalia

128 imulates kidney progenitor cells to form new nephrons is not known.

129 tion of the functional filtration units, the nephrons, is essential for postnatal life.

130 direct and indirect effects on ENaC, distal nephron K(+) channels, and WNK signaling.

131 Moreover, at the single-nephron level, diabetes-related renal hemodynamic altera

132 of hPSCs into kidney tissues, termed induced nephron-like organoids (iNephLOs).

133 In the ageing kidney there is nephron loss and lesions of focal glomerulosclerosis, in

134 mediated by infiltrating leukocytes leads to nephron loss and renal fibrosis, typical hallmarks of ch

135 xpression changes in response to progressive nephron loss or whether APA exerts a protective role aga

136 The incomplete representation of nephron loss with aging by either increased glomeruloscl

137 n chronic glomerular disease and consecutive nephron malfunction.

138 -as an adaptation to reduction in functional nephron mass and/or in response to prevailing metabolic

139 rationale for therapies aimed at increasing nephron mass.

140 dosimetry based on alpha-camera images and a nephron model revealed hot spots in the proximal renal t

141 on and results in a substantial reduction of nephron number as well as renal hypoplasia at birth.

142 esults support the feasibility of estimating nephron number by a combination of unenhanced CT and bio

143 In donors, estimated nephron number by unenhanced CT was consistent with that

144 Methods for estimating nephron number in a clinical setting may be useful for p

145 In conclusion, lower nephron number in healthy adults associates with charact

146 Nephron number is a major determinant of long-term renal

147 The decline of nephron number is accompanied by a comparable reduction

148 Nephron number may be an important determinant of kidney

149 on complement can vary 10-fold, with reduced nephron number predisposing individuals to hypertension,

150 Low nephron number results in an increased risk of developin

151 Nephrosclerosis, nephron size, and nephron number vary among kidneys transplanted from livi

152 Nephron number was determined as the product of cortical

153 rophy, larger cortical nephron size (but not nephron number), and smaller medullary volume.

154 Nephron number, as assessed by gold standard stereologic

155 Mutation in frizzled9b reduced total kidney nephron number, caused defects in tubule morphology and

156 e and glomerular density on biopsy to assess nephron number.

157 itional factors during gestation and reduced nephron number.

158 e concentration and the number of developing nephrons observed in the posterior kidney.

159 rom Bowman space to the papillary tip of the nephron of a human kidney.

160 rin 2-positive principal cells of the distal nephron of adult human kidney.

161 The distal nephrons of females had a higher abundance of total and

162 egulation of miR-466 was confirmed in distal nephrons of mice on low Na(+) diets.

163 Drug precipitation in the nephrons of the kidney can cause drug-induced crystal ne

164 progenitor cells (NPCs) generate all of the nephrons of the mammalian kidney during development.

165 GFR was independently associated with larger nephrons on biopsy and more glomerulosclerosis and arter

166 rived models of kidney tissue either contain nephrons or pattern specifically to the ureteric epithel

167 The genetic regulation of nephron patterning during kidney organogenesis remains p

168 Malpighian tubules, analogous to vertebrate nephrons, play a key role in insect osmoregulation and d

169 ing nephron; and tubule fusion where the new nephron plumbs into the distal tubule and establishes bl

170 These studies suggest that nephron polycystin-1 deficiency does not itself contribu

171 to describe a potential physiologic role for nephron polycystin-1 in the absence of cysts, tubule dil

172 ike cells, were able to repopulate different nephron portions of renal extracellular matrix scaffolds

173 n the nephrogenic lineage results in loss of nephron progenitor cell (NPC) renewal, a phenotype oppos

174 hages, we identify a role for macrophages in nephron progenitor cell clearance as mouse kidney develo

175 nases restrict Yap/Taz activities to promote nephron progenitor cell differentiation in the mammalian

176 valuate Troy/TNFRSF19 as a segment-committed nephron progenitor cell marker.

177 By embryonic day 15.5, kidneys of nephron progenitor cell-specific VHL knockout mice begin

178 Deletion of Dnmt1 in nephron progenitor cells (in contrast to deletion of Dnm

179 velop a high-efficiency protocol to generate nephron progenitor cells (NPCs) and kidney organoids to

180 Transit-amplifying nephron progenitor cells (NPCs) generate all of the neph

181 SIX2 (SIX homeobox 2)-positive nephron progenitor cells (NPCs) give rise to all epithel

182 Nephron progenitor cells (NPCs) give rise to all segment

183 Nephron progenitor cells (NPCs) show an age-dependent ca

184 ith genetic deletion of Dnmt3a and Dnmt3b in nephron progenitor cells (Six2 (Cre) Dnmt3a/3b) and kidn

185 cation methylcytosine hydroxylases (Tet2) in nephron progenitor cells (Six2 (Cre)) in mice.

186 accumulated in the interstitium derived from nephron progenitor cells and expressed E-cadherin as wel

187 sly we discovered that, once Six2-expressing nephron progenitor cells and Foxd1-expressing renal inte

188 e-cell RNA sequencing identifies a subset of nephron progenitor cells as a potential source of renal

189 se data suggest that Pax2 function maintains nephron progenitor cells by repressing a renal interstit

190 Little is known about how multipotent nephron progenitor cells differentiate into different ne

191 tments is maintained by the Pax2 activity in nephron progenitor cells during kidney organogenesis.

192 We demonstrate that nephron progenitor cells lacking Pax2 fail to differenti

193 ted allele of beta-catenin in the stromal or nephron progenitor cells reveals that human WT more clos

194 C, differentiated hPSCs into SIX2(+)SALL1(+) nephron progenitor cells with 92% efficiency within 2 da

195 transcriptional coactivators Yap and Taz, in nephron progenitor cells.

196 ewing and differentiating populations of the nephron progenitor cells.

197 uRD) to inhibit premature differentiation of nephron progenitor cells.

198 ensure proliferation and differentiation of nephron progenitor cells.

199 s identify a novel role for VHL in mediating nephron progenitor differentiation through metabolic reg

200 up-regulation of Foxd1, a known regulator of nephron progenitor differentiation.

201 mined by the self-renewal and induction of a nephron progenitor pool established at the onset of kidn

202 To explore VHL as a regulator defining nephron progenitor self-renewal versus differentiation,

203 at miRNA-mediated regulation of Bim controls nephron progenitor survival during nephrogenesis, as one

204 Bim gene dosage is critical in modulating nephron progenitor survival in the absence of microRNAs

205 PSCs to the mouse metanephric mesenchyme, a nephron progenitor.

206 Furthermore, 2 miRNAs expressed in nephron progenitors (miR-17 and miR-106b) regulated Bim

207 In wild-type mice, p-Creb marked nephron progenitors (NP), early epithelial NP derivative

208 VHL knockout nephron progenitors also exhibit persistent Six2 and Wt1

209 ) resulted in accelerated differentiation of nephron progenitors and bilateral renal hypoplasia.

210 loss of Bim partially restored the number of nephron progenitors and improved nephron formation.

211 a stable form of beta-catenin in epithelial nephron progenitors blocked the proper formation of all

212 egulatory actions of Six2 in mouse and human nephron progenitors by chromatin immunoprecipitation fol

213 al modelling of returning cells reveals that nephron progenitors can traverse the transcriptional hie

214 stitutive activation of Notch in mesenchymal nephron progenitors causes ectopic expression of Lhx1 an

215 he maintenance and commitment of mesenchymal nephron progenitors during kidney development.

216 n of all nephron segments and that it primes nephron progenitors for differentiation rather than dire

217 n and gain-of-function studies in epithelial nephron progenitors in the mouse kidney.

218 We also found that epithelial nephron progenitors lacking beta-catenin failed to form

219 Interestingly, we found that epithelial nephron progenitors lacking beta-catenin were able to fo

220 Genetic deletion of Lats1 and Lats2 in nephron progenitors of mice led to disruption of nephrog

221 We show in mice that differentiation of nephron progenitors requires downregulation of Six2, a t

222 icroRNA (miRNA)-processing enzyme Dicer from nephron progenitors results in premature depletion of th

223 During mammalian kidney development, nephron progenitors undergo a mesenchymal-to-epithelial

224 how it regulates nephron segmentation after nephron progenitors undergo mesenchymal-to-epithelial tr

225 ogress to mesoderm precursors, proliferative nephron progenitors, and eventually become mature podocy

226 nce reporter iPSC lines designed to identify nephron progenitors, podocytes, proximal and distal neph

227 Nephron progenitors, the cell population that give rise

228 ntial for the renewal and differentiation of nephron progenitors.

229 h a conditional deletion of VHL from Six2(+) nephron progenitors.

230 mice begin to exhibit reduced maturation of nephron progenitors.

231 ing a circuit of autoregulation operating in nephron progenitors.

232 genetic deletion leads to a rapid decline of nephron progenitors.

233 increased Bim expression in Dicer-deficient nephron progenitors.

234 myofibroblastic cells can differentiate from nephron progenitors.

235 g from the cortex, where they connect to the nephron proper, into the medulla, where they release uri

236 Nephron reduction caused Stat3 phosphorylation in tubula

237 The formation of the proper number of nephrons requires a tightly regulated balance between re

238 lium and no ureteric epithelium, this distal nephron segment alone displays significant in vitro plas

239 The precise transcriptional changes in this nephron segment during fibrosis and potential difference

240 ion of Tfap2a and Kctd15 kinetics to control nephron segment fate choice and differentiation during k

241 on transport and endocytic functions of this nephron segment.

242 n directing their cell fates into a specific nephron segment.

243 it is not fully understood how it regulates nephron segmentation after nephron progenitors undergo m

244 To investigate whether Notch regulates nephron segmentation, we performed Notch loss-of-functio

245 regulation of beta-catenin signaling during nephron segmentation.

246 -catenin regulates the formation of multiple nephron segments along the proximo-distal axis of the ma

247 of a Notch signaling inhibitor in all of the nephron segments and collecting ducts in mice after kidn

248 ibition of Notch blocks the formation of all nephron segments and that constitutive activation of Not

249 gnaling is required for the formation of all nephron segments and that it primes nephron progenitors

250 that orchestrate differentiation of specific nephron segments are incompletely understood, and the fa

251 Exosomes derived from all nephron segments are present in human urine, where their

252 elective inactivation of Sec63 in all distal nephron segments in embryonic mouse kidney results in po

253 THP-, NKCC2- and AQP1-positive loop of Henle nephron segments in mutant DeltaSRM kidneys.

254 ecular transition states along more than ten nephron segments spanning two major kidney regions.

255 found to be expressed differentially across nephron segments with the highest expression in the inne

256 Because pon-2 mRNA resides in multiple rat nephron segments, including the aldosterone-sensitive di

257 tochondrial function in intact tissue in all nephron segments, may provide new insights into how the

258 elative proportion of proximal versus distal nephron segments, producing a correlative level of vascu

259 genitors blocked the proper formation of all nephron segments, suggesting tight regulation of beta-ca

260 sion of genes for renal progenitor-cells and nephron segments.

261 es comprising tubular epithelia of different nephron segments.

262 he specialized metabolic functions of distal nephron segments.

263 rogenitor cells differentiate into different nephron segments.

264 dgehog pathway in epithelial cells along the nephron significantly influenced the severity of the pol

265 al fibrosis/tubular atrophy, larger cortical nephron size (but not nephron number), and smaller medul

266 Nephrosclerosis, nephron size, and nephron number vary among kidneys tran

267 Subclinical nephrosclerosis, larger cortical nephron size, and smaller medullary volume in healthy do

268 mean cross-sectional tubular area to measure nephron size; and calculations from CT cortical volume a

269 We generated adult inducible nephron-specific alphaENaC-knockout mice (Scnn1a(Pax8/LC

270 We induced nephron-specific disruption of the Pkd1 gene in 3-month-

271 Nephron-specific TrkC knockout (TrkC-KO) and nephron-spe

272 Nephron-specific TrkC knockout (TrkC-KO) and nephron-specific TrkC-overexpressing (TrkC-OE) mice were

273 Here, we demonstrate that embryonic-stage, nephron-specific Tulp3 knockout mice developed cystic ki

274 osition of nephrons dependent on the time of nephron specification, and lineage convergence, in which

275 In the Spare-the-Nephron (STN) Study, kidney transplant recipients random

276 ed Ncam1, Pax2, and Sox9 markers of immature nephron structures and dedifferentiated proximal tubules

277 ed SALL1 expression and marked dysgenesis of nephron structures were observed in the rudimentary kidn

278 he kidney contains the functional units, the nephrons, surrounded by the renal interstitium.

279 ive rise to all epithelial cell types of the nephron, the filtering unit of the kidney.

280 ls give rise to the distinct segments of the nephron, the functional unit of the kidney.

281 em cells to replace damaged tubules with new nephrons: the filtration units of the kidney.

282 ms (Epac1 and Epac2) are expressed along the nephron, their relevance in the kidney remains obscure.

283 D1 axis links a developmental pathway in the nephron to the induction and maintenance of terminal dif

284 Nephron tubules in zebrafish are composed of segment pop

285 n vivo examination of early-stage developing nephron tubules reveals that cell division is not orient

286 orientation of apical-basal cell division in nephron tubules.

287 Renal functional units known as nephrons undergo patterning events during development th

288 e cell types including the collecting ducts, nephrons, vasculature and interstitium.

289 ment, distinct progenitors contribute to the nephrons versus the ureteric epithelium of the kidney.

290 we found that HIF activation in the proximal nephron via induced inactivation of the von Hippel-Linda

291 s 115+/-24 ml per minute, the mean number of nephrons was 860,000+/-370,000 per kidney, and the mean

292 controls, whereas TMPRSS2 (primarily distal nephron) was highest in telmisartan-treated animals.

293 formation of distal tubules in the mammalian nephron, we show that inhibition of Notch blocks the for

294 cells of mouse aldosterone-sensitive distal nephron where ENaC is localized.

295 , including the aldosterone-sensitive distal nephron where the epithelial Na(+) channel (ENaC) is exp

296 being expressed in the distal aspects of the nephron, where ENaCs couple the absorption of filtered N

297 es contain proteins from all sections of the nephron, whereas most studied circulating extracellular

298 ate kidney relies on structural units called nephrons, which are epithelial tubules with a sequence o

299 events that induce renal progenitors to form nephrons with an intricate composition of multiple segme

300 ken to be the same between the human and rat nephrons (with the exception of a glucose transporter al