Abstract

Over the past few years, tremendous advances have occurred in stem cell biology. With the development of induced pluripotent stem cell technology, it is now possible to reprogram adult cells to differentiate into multiple cell types, including renal cells.1 Although induced pluripotent stem cells hold great promise for treatment of chronic diseases such as kidney failure in the future, current therapies are limited to readily available endogenous progenitor cell populations that can be isolated or mobilized from the bone marrow. These include hematopoietic stem cells (HSCs), mesenchymal stem cells, and endothelial progenitor cells, collectively known as bone marrow–derived cells (BMDCs). Therapies to enhance mobilization of endogenous BMDCs or infusions of BMDCs have been used in preclinical models of renal disease that include ischemia-reperfusion injury, the Thy1.1 model of mesangial proliferative glomerulonephritis, renovascular disease, and Alport syndrome, to name a few.2–10 Improved renal outcomes were reported in a number of these studies, although it is debated whether this is the result of cytokines or secreted factors produced by the BMDCs or the consequence of transdifferentiation of BMDCs into specific renal cell types. In regard to the latter, studies suggested variable abilities of these cells to transdifferentiate into renal endothelial, tubular, and glomerular epithelial cell lineages. Although it is not uniformly accepted that true transdifferentiation from BMDCs occurs, most agree that if it does occur, then it contributes only a small proportion of cells to the kidney. In the renal clinical …

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