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2014 ; 34
(4
): 404-17
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Defining the acute kidney injury and repair transcriptome
#MMPMID25217269
Kumar S
; Liu J
; McMahon AP
Semin Nephrol
2014[Jul]; 34
(4
): 404-17
PMID25217269
show ga
The mammalian kidney has an intrinsic ability to repair after significant injury.
However, this process is inefficient: patients are at high risk for the loss of
kidney function in later life. No therapy exists to treat established acute
kidney injury (AKI) per se: strategies to promote endogenous repair processes and
retard associated fibrosis are a high priority. Whole-organ gene expression
profiling has been used to identify repair responses initiated with AKI, and
factors that may promote the transition from AKI to chronic kidney disease.
Transcriptional profiling has shown molecular markers and potential regulatory
pathways of renal repair. Activation of a few key developmental pathways has been
reported during repair. Whether these are comparable networks with similar target
genes with those in earlier nephrogenesis remains unclear. Altered microRNA
profiles, persistent tubular injury responses, and distinct late inflammatory
responses highlight continuing kidney pathology. Additional insights into injury
and repair processes will be gained by study of the repair transcriptome and
cell-specific translatome using high-resolution technologies such as RNA
sequencing and translational profiling tailored to specific cellular compartments
within the kidney. An enhanced understanding holds promise for both the
identification of novel therapeutic targets and biomarker-based evaluation of the
damage-repair process.