Stem cells in action: addressing ischemia-reperfusion injury in acute kidney injury.

Acute kidney injury (AKI), which is the most frequent cause of transitory or prolonged renal hypoperfusion called ischemia-reperfusion injury (IRI), is characterized by an acute inflammatory response, tubular necrosis, programmed cell death, and shedding of epithelial cells into the tubular lumen. Unfortunately, the pathophysiology of IRI is multifactorial and only partially understood. IRI is a pathological condition that may be responsible for various changes, such as structural and functional changes in epithelial cells and changes in the interstitium (inflammation and microvasculopathy). Even though studies suggest that stem cells (SC) can play an important role during kidney repair; they also suggest that they aid in regeneration and provide possible therapeutic modalities. These cells may be derived from different sources, including bone marrow (BM) or kidney. Two important characteristics of these cells are their ability to undergo transdifferentiation into tubular cells and/or to fuse with endothelial cells. The proliferation of dedifferentiated cells can significantly contribute to tissue regeneration. Mature kidney cells that participate in repairing kidney damage, typically differentiate from renal stem cells that have migrated to the location of kidney regeneration or from bone marrow stem cells accessible to the injured epithelium. However, only a small percentage of SC from BM stably integrates into the endothelial and/or tubular epithelial cells. Although SC therapy shows remarkable benefits in IRI, most findings come from small experimental models, indicating that further exploration is necessary. On the other hand majority of authors show no benefit of SC in renal IRI. Aim of this review is to evaluate importance of stem cells in repair of renal IRI.