The Study of Angptl4-Modulated Podocyte Injury in IgA Nephropathy
Increasing evidence shows that Angptl4 affects proteinuria in podocytes injured kidney disease, however, whether there is a relationship between Angptl4 and IgA nephropathy (IgAN) has not been studied yet. Plasma and urine samples were obtained from 71 patients with IgAN and 61 healthy controls. Glo...
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Published in | Frontiers in physiology Vol. 11; p. 575722 |
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Main Authors | , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
Frontiers Media S.A
11.02.2021
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Subjects | |
Online Access | Get full text |
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Summary: | Increasing evidence shows that Angptl4 affects proteinuria in podocytes injured kidney disease, however, whether there is a relationship between Angptl4 and IgA nephropathy (IgAN) has not been studied yet.
Plasma and urine samples were obtained from 71 patients with IgAN and 61 healthy controls. Glomeruli from six renal biopsy specimens (three IgAN patients and three healthy controls) were separated by RNA-Seq. Differentially expressed genes (DEGs) related to podocytes and Angptl4 between IgAN patients and healthy controls were performed using the Limma package. Gene set enrichment analysis was used to determine whether there was a statistically significant difference between the two groups. STRING was used to create a protein-protein interaction network of DEGs. Association analysis between Angptl4 levels and clinical features of IgAN was performed.
Thirty-three podocyte-related and twenty-three Angpt4-related DEGs were found between IgAN patients and healthy controls. By overlapping the genes,
and
were found to be upregulated in IgAN patients, while
was downregulated in IgAN patients. Plasma and urine Angptl4 levels were closely related to the degree of podocyte injury and urine protein, but not to the protein-creatine ratio.
Our findings show that Angptl4 levels in plasma and urine are related to podocyte damage and, therefore, may be a promising tool for assessing the severity of IgAN patients to identify and reverse the progression to ESRD. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Reviewed by: Oleg Palygin, Medical College of Wisconsin, United States; Vladimir Tesar, Charles University, Czechia This article was submitted to Renal and Epithelial Physiology, a section of the journal Frontiers in Physiology These authors have contributed equally to this work Edited by: Xueying Zhao, Morehouse School of Medicine, United States |
ISSN: | 1664-042X 1664-042X |
DOI: | 10.3389/fphys.2020.575722 |