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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.
34 re released from all regions of the kidney's nephron and from other cells that line the urinary tract
36 for Na(+) reabsorption in the distal kidney nephron and is regulated by numerous hormones, including
40 define sexual dimorphic phenotypes along the nephron and suggest that lower proximal reabsorption in
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
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
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
65 -fold higher in the advanced DKD population (NEPHRON-D) than in the early DKD population (ACCORD).
68 exacerbated cystogenesis and caused drastic nephron damage and renal fibrosis, leading to kidney fai
70 n hypothesized to predispose to irreversible nephron damage, thereby contributing to initiation and p
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
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
87 enewal target assessed as well as for proper nephron endowment in vivo This study suggests that, with
92 s for understanding the pathways that affect nephron epithelial cells during kidney disease and regen
95 r the first time that PGE2 is a regulator of nephron formation in the zebrafish embryonic kidney, thu
99 pulation within the intermediate mesoderm to nephron-forming cell fates and a common origin shared be
102 the function of all nephrons, and the single-nephron GFR assesses the function of individual nephrons
110 mong healthy adult kidney donors, the single-nephron GFR was fairly constant with regard to age, sex,
116 thin the aldosterone-sensitive region of the nephron, i.e., the distal convoluted tubule, the connect
119 vise strategies to stimulate regeneration of nephrons in situ to restore failing kidney function.
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
125 brafish embryo undergo tubulogenesis to form nephrons is poorly understood, but is known to involve a
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
131 ion differentiates spheroids into segmented, nephron-like kidney organoids containing cell population
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
137 are associated with exaggerated age-related nephron loss, probably decaying from a larger pool of sm
139 -as an adaptation to reduction in functional nephron mass and/or in response to prevailing metabolic
141 dosimetry based on alpha-camera images and a nephron model revealed hot spots in the proximal renal t
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
148 ritical for normal nephron number, while low nephron number is implicated in hypertension and renal d
150 cting duct system and is critical for normal nephron number, while low nephron number is implicated i
152 irment because of the combination of reduced nephron numbers and prolonged exposure to renal compensa
155 ption of water from the luminal fluid of the nephron occurs through aquaporin-2 (AQP2) water pores in
158 progenitor cells (NPCs) generate all of the nephrons of the mammalian kidney during development.
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
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
172 nases restrict Yap/Taz activities to promote nephron progenitor cell differentiation in the mammalian
174 velop a high-efficiency protocol to generate nephron progenitor cells (NPCs) and kidney organoids to
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.
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.
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
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
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.
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
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.
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
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
234 g from the cortex, where they connect to the nephron proper, into the medulla, where they release uri
236 Here, we combined an experimental model of nephron reduction in mice from different genetic backgro
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
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
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
264 y reviewed our institutional experience with nephron sparing surgery (NSS) in patients with synchrono
266 r time (from 69.0% to 42.5%), and the use of nephron-sparing surgery (partial nephrectomy and ablatio
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
276 ed Ncam1, Pax2, and Sox9 markers of immature nephron structures and dedifferentiated proximal tubules
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
283 beta-catenin activity, we force cells within nephrons to differentiate according to the imposed beta-
285 n vivo examination of early-stage developing nephron tubules reveals that cell division is not orient
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
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
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
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