This chapter reviews some reports which indicate that the MSCs directly replace dead tubular epithelial, whereas other observations suggest that MSCs regulate the endogenous reparative machinery without transdifferentiating into tubular cells overall, the emerging body of evidence describing MSC modulation of acute kidney injury (AKI) has stimulated a reappraisal of the cellular mechanisms behind renal injury and repair as well as generated considerable excitement at the prospects for novel cell therapies to treat human kidney diseases. Stem cells play fundamental roles in the self-renewal of adult tissues throughout life. Some tissues are characterized by ongoing loss of cells, including the hematopoietic system, intestine and skin, and adult stem cells are responsible for replenishing these cells to maintain tissue homeostasis. Other organs, such as kidney or lung, have a much lower rate of cellular turnover, but are capable of proliferating and repairing after an injury stimulus. Based on the high proliferative capacity of injured kidney, one longstanding model holds that tubular cells themselves are the source of nephron repair. Studies on the role of bone marrow-derived cells (BMDCs) initially challenged this model of dedifferentiation followed by proliferation and redifferentiation of existing tubular cells after injury. While it has long been appreciated that bone marrow-derived inflammatory cells home to injured kidney, recent studies have suggested that BMDCs directly participate in renal injury and repair. MSCs in particular have been reported to protect against experimental renal injury as well as accelerate the repair process in rodent models.

Original languageEnglish
Title of host publicationRegenerative Nephrology
Number of pages14
ISBN (Electronic)9780123809285
StatePublished - Jan 1 2011


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