Abstract:
: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.
journal_name
Nat Communjournal_title
Nature communicationsauthors
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,Ladoi
10.1038/s41467-018-03753-4subject
Has Abstractpub_date
2018-04-09 00:00:00pages
1344issue
1issn
2041-1723pii
10.1038/s41467-018-03753-4journal_volume
9pub_type
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