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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Nat+Commun
2018 ; 9
(1
): 1344
Nephropedia Template TP
gab.com Text
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English Wikipedia
Endocycle-related tubular cell hypertrophy and progenitor proliferation recover
renal function after acute kidney injury
#MMPMID29632300
Lazzeri E
; Angelotti ML
; Peired A
; Conte C
; Marschner JA
; Maggi L
; Mazzinghi B
; Lombardi D
; Melica ME
; Nardi S
; Ronconi E
; Sisti A
; Antonelli G
; Becherucci F
; De Chiara L
; Guevara RR
; Burger A
; Schaefer B
; Annunziato F
; Anders HJ
; Lasagni L
; Romagnani P
Nat Commun
2018[Apr]; 9
(1
): 1344
PMID29632300
show ga
Acute kidney injury (AKI) is considered largely reversible based on the capacity
of surviving tubular cells to dedifferentiate and replace lost cells via cell
division. Here we show by tracking individual tubular cells in conditional
Pax8/Confetti mice that kidney function is recovered after AKI despite
substantial tubular cell loss. Cell cycle and ploidy analysis upon AKI in
conditional Pax8/FUCCI2aR mice and human biopsies identify endocycle-mediated
hypertrophy of tubular cells. By contrast, a small subset of Pax2+ tubular
progenitors enriches via higher stress resistance and clonal expansion and
regenerates necrotic tubule segments, a process that can be enhanced by suitable
drugs. Thus, renal functional recovery upon AKI involves remnant tubular cell
hypertrophy via endocycle and limited progenitor-driven regeneration that can be
pharmacologically enhanced.