A number of genes involved in kidney development are reactivated in the adult after acute kidney injury (AKI). This has led to the belief that tissue repair mechanisms recapitulate pathways involved in embryonic development after AKI. We will discuss evidence to support this hypothesis by comparing the mechanisms of development with common pathways known to regulate post-AKI repair, or that we identified as cell-specific candidates based on public datasets from recent AKI translational profiling studies. We will argue that while many of these developmental pathways are reactivated after AKI, this is not associated with general cellular reprogramming to an embryonic state. We will show that reactivation of these developmental genes is often associated with expression in cells that are not normally involved in mediating parallel responses in the embryo, and that depending on the cellular context, these responses can have beneficial or detrimental effects on injury and repair after AKI.
Keywords: Acute kidney injury; embryonic development; endothelial cells; fibroblasts; ischemia reperfusion; macrophages; regeneration; tissue repair; translational profiling; tubular epithelial cells; vascular pericytes.