ArticleThe American journal of pathology2010
Human nephrosclerosis triggers a hypoxia-related glomerulopathy.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 104 citations in OpenAlex.
- Urate-lowering therapy for CKD patients with asymptomatic hyperuricemia without proteinuria elucidated by attribute-based research in the FEATHER Study.Scientific reports · 2022Trial
- Construction and validation of a hypertensive nephropathy diagnostic model based on mitochondrial-related genes using machine learning combined with WGCNA.International urology and nephrology · 2026Article
- Hypoxia inducible factor network reflects kidney disease progression in diabetes and sodium-glucose co-transporters inhibition.Signal transduction and targeted therapy · 2026Article
- Shared multicellular injury programs of acute and chronic kidney disease enable mechanistic patient stratification.medRxiv : the preprint server for health sciences · 2026Article
- The intelligent podocyte: sensing and responding to a complex microenvironment.Nature reviews. Nephrology · 2025Review
- Assessing Creatine-Related Gene Expression in Kidney Disease: Can Available Data Give Insights into an Old Discussion?Nutrients · 2025Review
- Zyxin is important for the stability and function of podocytes, especially during mechanical stretch.Communications biology · 2024Article
- SCARF Genes in COVID-19 and Kidney Disease: A Path to Comorbidity-Specific Therapies.International journal of molecular sciences · 2023Review
- Exploring the Interplay between Polyphenols and Lysyl Oxidase Enzymes for Maintaining Extracellular Matrix Homeostasis.International journal of molecular sciences · 2023Review
- Stem Cells in Kidney Ischemia: From Inflammation and Fibrosis to Renal Tissue Regeneration.International journal of molecular sciences · 2023Review
- Differentially Expressed Genes and Molecular Susceptibility to Human Age-Related Diseases.International journal of molecular sciences · 2023Article
- Assessment of Fibrinogen-like 2 (FGL2) in Human Chronic Kidney Disease through Transcriptomics Data Analysis.Biomolecules · 2022Article
- Kidney Injuries and Evolution of Chronic Kidney Diseases Due to Neonatal Hyperoxia Exposure Based on Animal Studies.International journal of molecular sciences · 2022Review
- Dissecting signalling pathways associated with intrarenal synthesis of complement components in lupus nephritis.RMD open · 2022Article
- Emerging Roles for G Protein-Coupled Estrogen Receptor 1 in Cardio-Renal Health: Implications for Aging.Biomolecules · 2022Review
- Stress Reactivity, Susceptibility to Hypertension, and Differential Expression of Genes in Hypertensive Compared to Normotensive Patients.International journal of molecular sciences · 2022Article
- Potential Involvement of Complement Activation in Kidney Vascular Lesions of Arterionephrosclerosis.Frontiers in medicine · 2022Article
- Identification of an Altered Matrix Signature in Kidney Aging and Disease.Journal of the American Society of Nephrology : JASN · 2021Article
- The unique molecular mechanism of diabetic nephropathy: a bioinformatics analysis of over 250 microarray datasets.Clinical kidney journal · 2021Article
- Bioinformatics Analysis Reveals Crosstalk Among Platelets, Immune Cells, and the Glomerulus That May Play an Important Role in the Development of Diabetic Nephropathy.Frontiers in medicine · 2021Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 6 institutions in 3 countries.
Funding
Abstract
In the kidney, hypoxia contributes to tubulointerstitial fibrosis, but little is known about its implications for glomerular damage and glomerulosclerosis. Chronic hypoxia was hypothesized to be involved in nephrosclerosis (NSC) or "hypertensive nephropathy." In the present study genome-wide expression data from microdissected glomeruli were studied to examine the role of hypoxia in glomerulosclerosis of human NSC. Functional annotation analysis revealed prominent regulation of hypoxia-associated biological processes in NSC, including angiogenesis, fibrosis, and inflammation. Glomerular expression levels of a majority of genes regulated by the hypoxia-inducible factors (HIFs) were significantly altered in NSC. Among these HIF targets, chemokine C-X-C motif receptor 4 (CXCR4) was prominently induced. Glomerular CXCR4 mRNA induction was confirmed by quantitative RT-PCR in an independent cohort with NSC but not in those with other glomerulopathies. By immunohistological analysis, CXCR4 showed enhanced positivity in podocytes in NSC biopsy specimens. This CXCR4 positivity was associated with nuclear localization of HIF1alpha only in podocytes of NSC, indicating transcriptional activity of HIF. As the CXCR4 ligand CXCL12/SDF-1 is constitutively expressed in podocytes, autocrine signaling may contribute to NSC. In addition, a blocking CXCR4 antibody caused significant inhibition of wound closure by podocytes in an in vitro scratch assay. These data support a role for CXCR4/CXCL12 in human NSC and indicate that hypoxia not only is involved in tubulointerstitial fibrosis but also contributes to glomerular damage in NSC.
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