ライフサイエンスコーパス: nephron

1 nd defines the 'aldosterone-sensitive distal nephron'.

2 of approximately 1 million functional units (nephrons).

3 rect mineralocorticoid actions in the distal nephron.

4 egulates electrolyte transport in the distal nephron.

5 l in which FKBP12 could be deleted along the nephron.

6 in of alpha-intercalated cells in the distal nephron.

7 lanarian excretory system and the vertebrate nephron.

8 des regulated sodium transport in the distal nephron.

9 sicle, the first epithelial precursor of the nephron.

10 ling in principal cells of the distal kidney nephron.

11 limb and in the aldosterone-sensitive distal nephron.

12 rturbations that develop in this part of the nephron.

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

14 es a prostaglandin transporter in the distal nephron.

15 ical membrane-determining CRB complex in the nephron.

16 dimorphic pattern of transporters along the nephron.

17 hron GFR assesses the function of individual nephrons.

18 ryomegaly and dysfunction of hepatocytes and nephrons.

19 so leads to the assembly of highly segmented nephrons.

20 cells to regulate their differentiation into nephrons.

21 UMOD protein, which is normally secreted by nephrons.

22 ypoplastic with fewer generations of nascent nephrons.

23 sted by a decrease in the size and number of nephrons.

24 destroyed by cysts, hypothesized to obstruct nephrons.

25 eration and reduced the number of developing nephrons.

26 d between caudal mesonephric and metanephric nephrons.

27 ck ascending limbs of short- and long-looped nephrons.

28 rotic glomeruli and hypertrophy of remaining nephrons.

29 on endowment at birth and subsequent loss of nephrons.

30 Distal nephron acid secretion is mediated by highly specialized

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

32 Mice lacking FKBP12 along the nephron also maintained a normal relationship between pl

33 NAs exhibit segmental distribution along the nephron and CDs.

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

35 The different segments of the nephron and glomerulus in the kidney balance the process

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

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

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

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

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

41 o depends on the donor supply of functioning nephrons and adaptation in GFR of a single kidney.

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

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

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

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

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

47 ctive inhibition of AT1 receptors within the nephron as a promising intervention for protecting patie

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

49 t of Arl13b Deletion of Arl13b in the distal nephron at the perinatal stage led to a cilia biogenesis

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

51 attributed to sodium retention in the distal nephron, but 11betaHSD2 is also expressed in the brain.

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

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

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

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

56 In the distal nephron, claudins need to form cation barriers and chlor

57 erated kidney-like organoids - complete with nephrons, collecting ducts, stroma, and vasculature - fr

58 istent that ChRCC originates from the distal nephron compared with other kidney cancers with more pro

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

60 y this renal development process because its nephrons contain segments akin to other vertebrates, inc

61 The nephron cortical collecting duct (CCD) is composed of pr

62 Notably, low nephron count increases the risk for developing hyperten

63 the duration of nephrogenesis and the final nephron count.

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 exacerbated cystogenesis and caused drastic nephron damage and renal fibrosis, leading to kidney fai

69 rlying renal growth and renal growth-induced nephron damage remain poorly understood.

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

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

72 phrectomy (uni-x) in sheep, leading to a 30% nephron deficit.

73 rs amplifying kidney injury and accelerating nephron demise.

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

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

78 sights into the genetic pathways that direct nephron development, and may have implications for under

79 velopment, specifically in the regulation of nephron development, with subsequent consequences for re

80 nt can be induced to form tubules expressing nephron differentiation markers.

81 e expression of genes that mark the onset of nephron differentiation.

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

83 e different potassium channels in the distal nephron, encoded by the genes KCNJ1, KCNJ10, KCNJ16, KCN

84 al and differentiation ultimately determines nephron endowment and thus susceptibile to chronic kidne

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 Nephron endowment is regulated by progenitor availabilit

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

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

92 s for understanding the pathways that affect nephron epithelial cells during kidney disease and regen

93 contain cells of multiple lineages including nephron epithelial cells.

94 Under normal conditions, nephrons expressed few EGFP and RFP puncta, but ischemia

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

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

97 e number of nephron progenitors and improved nephron formation.

98 nephrogenesis is completed prenatally, with nephrons formed until 34 weeks of gestational age.

99 pulation within the intermediate mesoderm to nephron-forming cell fates and a common origin shared be

100 atopoiesis but, surprisingly, also preserved nephron function.

101 he Cl(-)/HCO3(-) exchanger pendrin in distal nephron function.

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 psy findings were correlated with the single-nephron GFR.

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

114 ever, the role of Per1 in other parts of the nephron has not been investigated.

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

116 thin the aldosterone-sensitive region of the nephron, i.e., the distal convoluted tubule, the connect

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

118 ssue because it is competent to generate the nephrons in response to Wnt signaling.

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

120 sis: growth, patterning, branching rate, and nephron induction.

121 elian hypertension indicates that the distal nephron influences the overall natriuretic efficiency.

122 of chimeric drMM cultures indicated that the nephron is not derived from a single progenitor cell.

123 In this study, we demonstrate that the early nephron is patterned by a gradient in beta-catenin activ

124 The nephron is the basic physiologic subunit of the mammalia

125 brafish embryo undergo tubulogenesis to form nephrons is poorly understood, but is known to involve a

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

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

128 nslational signatures were identified in the nephron, kidney interstitial cell populations, vascular

129 y enlarge and, through compression of intact nephrons, lead to a decline in kidney function over time

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

131 ion differentiates spheroids into segmented, nephron-like kidney organoids containing cell population

132 Nephron loss due to normal aging or renal surgery (CKD-S

133 mpensatory programs initiated in response to nephron loss evoke glomerular hypertrophy, but not de no

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

135 nover and regeneration in repair, aging, and nephron loss remains unclear.

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

137 are associated with exaggerated age-related nephron loss, probably decaying from a larger pool of sm

138 podocytes in aging kidneys or in response to nephron loss.

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

140 results in hypoplastic kidneys with reduced nephron mass due to premature depletion of NPCs.

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

142 und the ureteric bud tips, and impairment of nephron morphogenesis.

143 The HSRA model is characterized by reduced nephron number (more than would be expected by loss of o

144 gh kidneys of equal size can vary 10-fold in nephron number at birth, discovering what regulates such

145 of preexisting hypertension on living donor nephron number has not been established.

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

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

148 ritical for normal nephron number, while low nephron number is implicated in hypertension and renal d

149 Nephron number may be an important determinant of kidney

150 cting duct system and is critical for normal nephron number, while low nephron number is implicated i

151 , as is the source of a 10-fold variation in nephron number.

152 irment because of the combination of reduced nephron numbers and prolonged exposure to renal compensa

153 renal injury may be due, in part, to reduced nephron numbers.

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

155 ption of water from the luminal fluid of the nephron occurs through aquaporin-2 (AQP2) water pores in

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

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

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

159 During fetal development, nephrons of the metanephric kidney form from a mesenchym

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

161 are amenable to gene targeting and can form nephron organoids that engraft in vivo, functionally cou

162 Little is known about nephron patterning during embryogenesis.

163 therefore identifies a molecular network for nephron patterning.

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

165 ing ducts (via HoxB7-Cre or Pax2-Cre) and in nephron precursors (via Pax2-Cre and Six2-Cre) resulted

166 Eya1, Pax2 and Bmp7 while the few surviving nephron precursors maintain expression of Wnt4, Lhx1, Pa

167 g the in vitro blood-perfused juxtamedullary nephron preparation.

168 th cultured mCCD and isolated primary distal nephron principal cells.

169 etween self-renewal and differentiation of a nephron progenitor cell (NPC) pool.

170 FGF, BMP, and WNT balance embryonic nephron progenitor cell (NPC) renewal and differentiatio

171 The balance between nephron progenitor cell (NPC) renewal, survival and diff

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

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

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

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

176 Self-renewal of nephron progenitor cells (NPCs) is governed by BMP, FGF

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

178 Conditional deletion of p53 in nephron progenitor cells (Six2Cre(+);p53(fl/fl)) induces

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

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

181 cap mesenchyme caused premature depletion of nephron progenitor cells and severe renal hypoplasia.

182 Self-renewal and proliferation of nephron progenitor cells and the decision to initiate ne

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

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

185 rter gene expression in the undifferentiated nephron progenitor cells in vivo.

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

187 trix, inhibiting BMP7-mediated transition of nephron progenitor cells to a compartment in which they

188 ired for the transition of CITED1-expressing nephron progenitor cells to a state that is primed for W

189 expressed in interstitial cells adjacent to nephron progenitor cells, suggesting an essential role f

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

191 ewing and differentiating populations of the nephron progenitor cells.

192 l or Vhl together with one allele of Bap1 in nephron progenitor cells.

193 tor, is required to maintain the stemness of nephron progenitor cells.

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

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

196 This in vitro nephron progenitor niche will have important application

197 thway is essential to the maintenance of the nephron progenitor niche.

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

199 53 in the maintenance of self-renewal of the nephron progenitor pool in the embryonic mouse kidney.

200 HS1) results in expansion of the mesenchymal nephron progenitor pool, called the condensing mesenchym

201 The nephron progenitor population was preserved in these mic

202 t have contributed to species differences in nephron progenitor programs such as the duration of neph

203 l, mesenchymal and ureteric) ensures correct nephron progenitor self-renewal and differentiation.

204 re dependent on Six2, a crucial regulator of nephron progenitor self-renewal.

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

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

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

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

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 with a conditional deletion of miR-17~92 in nephron progenitors and their derivatives.

212 l stem/progenitor cells expressed markers of nephron progenitors but also, stromal progenitors, with

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

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

215 uring nephrogenesis, multipotent mesenchymal nephron progenitors develop into distinct epithelial seg

216 ucial roles in Six2-dependent maintenance of nephron progenitors during mammalian nephrogenesis by st

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

218 Furthermore, we find that nephron progenitors lacking Notch signaling fail to diff

219 Deletion of all microRNAs (miRNAs) in nephron progenitors leads to premature loss of these cel

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

221 tumorigenesis are involved in the control of nephron progenitors or the microRNA (miRNA) processing p

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

223 tor receptor (Fgfr) docking protein in mouse nephron progenitors results in perinatal renal hypoplasi

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

225 ntified as a SIX2 target unique to the human nephron progenitors.

226 IX-factor regulation between mouse and human nephron progenitors.

227 Six1 and Six2 play non-overlapping roles in nephron progenitors.

228 IX1 and SIX2 activity in 16 week human fetal nephron progenitors.

229 redundant fashion to regulate the number of nephron progenitors.

230 ng the metabolic fitness and self-renewal of nephron progenitors.

231 -autonomously in the renal stroma to control nephron progenitors.

232 increased Bim expression in Dicer-deficient nephron progenitors.

233 myofibroblastic cells can differentiate from nephron progenitors.

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

235 Nephron reduction caused Stat3 phosphorylation in tubula

236 Here, we combined an experimental model of nephron reduction in mice from different genetic backgro

237 st proliferation and matrix synthesis, after nephron reduction.

238 A distal nephron remodeling process and induction of jagged 1/NOT

239 tudies in zebrafish revealed that pronephric nephrons require osr1 for proximal tubule and podocyte d

240 formation of the proper number of functional nephrons requires a delicate balance between renal proge

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

242 tor signaling in T lymphocytes or the distal nephron, respectively.

243 likely regulate claudins to fine-tune distal nephron salt transport.

244 Each nephron segment has distinct cell types and physiologica

245 Along this nephron segment, luminal delivery and transepithelial re

246 Using nephron segment-specific markers, we now show that tubul

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

248 on transport and endocytic functions of this nephron segment.

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

250 he permeability and selectivity of different nephron segments along the renal tubule.

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

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

253 Exosomes derived from all nephron segments are also present in human urine, where

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

255 , unique functions of any of the isoforms in nephron segments are still poorly understood.

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

257 by continuous sodium reabsorption in distal nephron segments with low water permeability, diuretic a

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

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

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

261 tch signaling fail to differentiate into any nephron segments, not just proximal tubules.

262 ity level, thereby causing spatial shifts in nephron segments.

263 se strain with Klotho deleted throughout the nephron (Six2-KL(-/-)).

264 y reviewed our institutional experience with nephron sparing surgery (NSS) in patients with synchrono

265 ney is an absolute indication for performing nephron-sparing surgery (NSS).

266 r time (from 69.0% to 42.5%), and the use of nephron-sparing surgery (partial nephrectomy and ablatio

267 The use of nephron-sparing surgery exceeds radical nephrectomy in p

268 g surgery, multiple absolute indications for nephron-sparing surgery still exist, including the class

269 tients who received surgical treatment, only nephron-sparing surgery was associated with a benefit in

270 the controversy surrounding the benefits of nephron-sparing surgery, multiple absolute indications f

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

272 Finally, nephron-specific Atp6ap2 depletion did not affect angiot

273 Taken together, our results show that nephron-specific deletion of Atp6ap2 does not affect the

274 chyme, a progenitor population distinct from nephron stem cells.

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

278 were lower in mice lacking FKBP12 along the nephron than in control mice.

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

280 urrent evidence for uEV signalling along the nephron, their role in health and disease of the kidney,

281 potassium channel KCNJ1 (ROMK) in the distal nephron, thereby contributing to the maintenance of pota

282 mice in which MRs could be deleted along the nephron to test this hypothesis.

283 beta-catenin activity, we force cells within nephrons to differentiate according to the imposed beta-

284 beta-catenin activity along the axis of the nephron tubule.

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 trafiltration coefficient (Kf) by the single-nephron ultrafiltration coefficient (SNKf).

288 Mutation in nephrons, ureteric smooth muscle, and mesenchyme surroun

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

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

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

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

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

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

295 on-A, non-B intercalated cells in the distal nephron, where it facilitates Cl(-) absorption and is in

296 essed by specific epithelial cells along the nephron, whereas expression of its receptor (Kdr/Vegfr2)

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

298 MR is highly expressed in the distal nephron, which is submitted to intense variations in ext

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

300 litate intercellular communication along the nephron, with the potential to change the function of th