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Cellular phenotypic transitions in diabetic nephropathy: An update

Affiliation
Department of Nephrology ,Union Hospital ,Tongji Medical College ,Huazhong University of Science and Technology ,Wuhan ,China
Cao, Yiling;
Affiliation
5th Medical Department ,Medical Faculty Mannheim ,University of Heidelberg ,Mannheim ,Germany
Lin, Ji-Hong;
Affiliation
5th Medical Department ,Medical Faculty Mannheim ,University of Heidelberg ,Mannheim ,Germany
Hammes, Hans-Peter;
Affiliation
Department of Nephrology ,Union Hospital ,Tongji Medical College ,Huazhong University of Science and Technology ,Wuhan ,China
Zhang, Chun

Diabetic nephropathy (DN) is a major cause of morbidity and mortality in diabetes and is the most common cause of end stage renal disease (ESRD). Renal fibrosis is the final pathological change in DN. It is widely believed that cellular phenotypic switching is the cause of renal fibrosis in diabetic nephropathy. Several types of kidney cells undergo activation and differentiation and become reprogrammed to express markers of mesenchymal cells or podocyte-like cells. However, the development of targeted therapy for DN has not yet been identified. Here, we discussed the pathophysiologic changes of DN and delineated the possible origins that contribute to myofibroblasts and podocytes through phenotypic transitions. We also highlight the molecular signaling pathways involved in the phenotypic transition, which would provide valuable information for the activation of phenotypic switching and designing effective therapies for DN.

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License Holder: Copyright © 2022 Cao, Lin, Hammes and Zhang.

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