Abstract
Podocytopathy is the most common feature of glomerular disorder characterized by podocyte injury- or dysfunction-induced excessive proteinuria, which ultimately develops into glomerulosclerosis and results in persistent loss of renal function. Due to the lack of self-renewal ability of podocytes, mild podocyte depletion triggers replacement and repair processes mostly driven by stem cells or resident parietal epithelial cells (PECs). In contrast, when podocyte recovery fails, activated PECs contribute to the establishment of glomerular lesions. Increasing evidence suggests that PECs, more than just bystanders, have a crucial role in various podocytopathies, including minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, diabetic nephropathy, IgA nephropathy, and lupus podocytopathy. In this review, we attempt to dissect the diverse role of PECs in the pathogenesis of podocytopathy based on currently available information.
Highlights
Glomerular visceral epithelial cells referred to as podocytes, are terminally differentiated cells found in the human body, containing a nucleus, and involved in primary processes, as well as foot processes (FPs)
There is currently no data to support the association of a disease with primary parietal epithelial cells (PECs) lesions, PECs are active in a variety of glomerular diseases, such as podocytopathies
PECs play a significant role in mechanosensation, contractility, glomerular barrier, and protein uptake but it seems likely that activated PECs serve as progenitor cells to replenish the decreased number of podocytes in podocytopathies, which provides an exciting idea to reverse the progression of human glomerular diseases
Summary
Zhi-hang Li†, Xiao-yan Guo†, Xiao-ying Quan†, Chen Yang, Ze-jian Liu, Hong-yong Su, Ning An* and Hua-feng Liu*. Specialty section: This article was submitted to Renal and Epithelial Physiology, a section of the journal Frontiers in Physiology. Podocytopathy is the most common feature of glomerular disorder characterized by podocyte injury- or dysfunction-induced excessive proteinuria, which develops into glomerulosclerosis and results in persistent loss of renal function. Due to the lack of self-renewal ability of podocytes, mild podocyte depletion triggers replacement and repair processes mostly driven by stem cells or resident parietal epithelial cells (PECs). When podocyte recovery fails, activated PECs contribute to the establishment of glomerular lesions. Increasing evidence suggests that PECs, more than just bystanders, have a crucial role in various podocytopathies, including minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, diabetic nephropathy, IgA nephropathy, and lupus podocytopathy. We attempt to dissect the diverse role of PECs in the pathogenesis of podocytopathy based on currently available information
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