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Tissue Culture Models of AKI: From Tubule Cells to Human Kidney Organoids.
Authors Bejoy J, Qian ES, Woodard LE
Submitted By Submitted Externally on 3/9/2022
Status Published
Journal Journal of the American Society of Nephrology : JASN
Year 2022
Date Published 3/1/2022
Volume : Pages 33 : 487 - 501
PubMed Reference 35031569
Abstract AKI affects approximately 13.3 million people around the world each year,
causing CKD and/or mortality. The mammalian kidney cannot generate new nephrons
after postnatal renal damage and regenerative therapies for AKI are not
available. Human kidney tissue culture systems can complement animal models of
AKI and/or address some of their limitations. Donor-derived somatic cells, such
as renal tubule epithelial cells or cell lines (RPTEC/hTERT, ciPTEC, HK-2,
Nki-2, and CIHP-1), have been used for decades to permit drug toxicity screening
and studies into potential AKI mechanisms. However, tubule cell lines do not
fully recapitulate tubular epithelial cell properties in situ when grown under
classic tissue culture conditions. Improving tissue culture models of AKI would
increase our understanding of the mechanisms, leading to new therapeutics. Human
pluripotent stem cells (hPSCs) can be differentiated into kidney organoids and
various renal cell types. Injury to human kidney organoids results in renal
cell-type crosstalk and upregulation of kidney injury biomarkers that are
difficult to induce in primary tubule cell cultures. However, current protocols
produce kidney organoids that are not mature and contain off-target cell types.
Promising bioengineering techniques, such as bioprinting and "kidney-on-a-chip"
methods, as applied to kidney nephrotoxicity modeling advantages and limitations
are discussed. This review explores the mechanisms and detection of AKI in
tissue culture, with an emphasis on bioengineered approaches such as human
kidney organoid models.


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