Abstract
Human kidney is particularly susceptible to ischemia and toxins with consequential tubular necrosis and activation of inflammatory processes. This process can lead to the acute renal injury, and even if the kidney has a great capacity for regeneration after tubular damage, in several circumstances, the normal renal repair program may not be sufficient to achieve a successful regeneration. Resident adult renal stem/progenitor cells could participate in this repair process and have the potentiality to enhance the renal regenerative mechanism. This could be achieved both directly, by means of their capacity to differentiate and integrate into the renal tissues, and by means of paracrine factors able to induce or improve the renal repair or regeneration. Recent genetic fate-tracing studies indicated that tubular damage is instead repaired by proliferative duplication of epithelial cells, acquiring a transient progenitor phenotype and by fate-restricted clonal cell progeny emerging from different nephron segments. In this review, we discuss about the properties and the reparative characteristics of high regenerative CD133+/CD24+ cells, with a view to a future application of these cells for the treatment of acute renal injury.
Highlights
Acute kidney injury (AKI) remains a major clinical event in nephrology with increasing incidence in both high- and low-income countries.[1]
AKI is characterized by acute tubular necrosis that is caused by three main factors: (1) sepsis, (2) nephrotoxicity, and (3) renal ischemia
The pathophysiological events occurring after tubular damage include molecular and cellular mechanisms that have been investigated by several studies,[3,4,5,6] but today the management of AKI is based on conservative therapy such as correction of reversible causes of kidney injury or dialytic treatment
Summary
Acute kidney injury (AKI) remains a major clinical event in nephrology with increasing incidence in both high- and low-income countries.[1]. The ARPCs can be isolated both from tubules and glomeruli; they have phenotypical and transcriptional characteristics that are very similar, but with some distinctive differences.[30,34] CD133+CD24+ tubular cells (tARPCs) are distinguished from CD133+CD24+ glomerular cells of the Bowman’s capsule (gARPCs) by the CD106 expression; they localize in the proximal tubule and in the connecting segment of tubules Both tARPCs and gARPCs regenerate tubular cells and improve renal function in SCID mice with AKI and proliferate following injury in the kidney of patients with acute or chronic tubular damage. It is still unclear whether renal function enhancement induced by progenitor cells is due to their differentiation and integration in the injured structures or to their paracrine effect
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