ArticleInternational journal of molecular sciences2021
CD73 Overexpression in Podocytes: A Novel Marker of Podocyte Injury in Human Kidney Disease.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Progression of diabetic nephropathy and adverse renal outcomes: possible involvement of Toll-like receptor 4 expression.Clinical and experimental nephrology · 2026Article
- Inhibiting the P2X7R-NLRP3 inflammasome pathway regulates CXCL16 to alleviate podocyte injury in mice with adriamycin nephropathy.Scientific reports · 2026Article
- Hypertension and age-related focal global glomerulosclerosis are associated with biomarkers for cellular senescence.Physiological reports · 2026Article
- A Case Report of Giant Congenital Melanocytic Nevus Complicated by Minimal Change Disease, With Genetic Analysis.Clinical case reports · 2025Article
- Identification of biomarkers related to immune and inflammation in membranous nephropathy: comprehensive bioinformatic analysis and validation.Frontiers in immunology · 2023Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The CD73 pathway is an important anti-inflammatory mechanism in various disease settings. Observations in mouse models suggested that CD73 might have a protective role in kidney damage; however, no direct evidence of its role in human kidney disease has been described to date. Here, we hypothesized that podocyte injury in human kidney diseases alters CD73 expression that may facilitate the diagnosis of podocytopathies. We assessed the expression of CD73 and one of its functionally important targets, the C-C chemokine receptor type 2 (CCR2), in podocytes from kidney biopsies of 39 patients with podocytopathy (including focal segmental glomerulosclerosis (FSGS), minimal change disease (MCD), membranous glomerulonephritis (MGN) and amyloidosis) and a control group. Podocyte CD73 expression in each of the disease groups was significantly increased in comparison to controls (
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