Dedifferentiation and Kidney System

Abstract

Renal cell dedifferentiation, redifferentiation, and proliferation could resort to kidney repair and regeneration both theoretically and practically. The vertebrate kidney has an intrinsic capability to regenerate following acute impairment. Impaired tubular epithelial cells’ rapid alternate and reconstitution of ordinary tubular role are required by the injured kidney’s successful regeneration. Identifying the cells participating in the regeneration process as well as the molecular mechanisms implicated may unveil therapeutic objectives for kidney disease’s therapy. Renal regeneration is connected with the expression of genetic pathways requisite for kidney organogenesis, indicating that the regenerating tubular epithelium may be “reprogrammed” to a less-differentiated, progenitor state. Proximal tubular cell and podocyte dedifferentiation serve as two critical approaches of regenerative medicine in nephrology. For acute kidney injury, proximal tubular cell damage is the main pathophysiological reason. The mechanism and morphological changes of proximal tubular cell dedifferentiation, redifferentiation, migration, and proliferation are articulated in this review. Several sorts of stem cells, like bone marrow-derived cells, adipocyte-derived mesenchymal stem cells, embryonic stem cells, and induced pluripotent stem cells, are utilized for renal regeneration in a similar way. Endogenous or lineage reprogrammed renal progenitor cells symbolize a magnetic probability for differentiation into multiple renal cell types. Additionally, podocyte dysfunction could bring about other categories of nephron-related disease, such as diabetic nephropathy and HIV-associated nephropathy. Interestingly, podocyte dedifferentiation is observed in the usual pathological process of HIV-associated nephropathy, which could provide an excellent research model for exploring underlying mechanism of podocyte differentiation.