ArticleFrontiers in pharmacology2019
CXCL6 Promotes Renal Interstitial Fibrosis in Diabetic Nephropathy by Activating JAK/STAT3 Signaling Pathway.
Article in Frontiers in pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 67 citations in OpenAlex.
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- Evaluation of toxicological mechanisms of ochratoxin-A in human primary proximal tubule epithelial cells.bioRxiv : the preprint server for biology · 2025Article
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- Causal inference of inflammatory proteins in infertility: a Mendelian randomization study.Frontiers in endocrinology · 2025Article
- Constructing the biomolecular networks associated with diabetic nephropathy and dissecting the effects of biomolecule variation underlying pathogenesis.Endocrine journal · 2024Article
- TMAO enhances TNF-α mediated fibrosis and release of inflammatory mediators from renal fibroblasts.Scientific reports · 2024Article
- Metabolic and inflammatory perturbation of diabetes associated gut dysbiosis in people living with and without HIV infection.Genome medicine · 2024Article
- Inflammation in diabetes complications: molecular mechanisms and therapeutic interventions.MedComm · 2024Review
- Landscape of infiltrating immune cells and related genes in diabetic kidney disease.Clinical and experimental nephrology · 2024Article
- Identification of potential diagnostic biomarkers associated with periodontitis by comprehensive bioinformatics analysis.Scientific reports · 2024Article
- Associations of inflammatory cytokines with palmoplantar pustulosis: a bidirectional Mendelian randomization study.Frontiers in medicine · 2024Article
- Potential Role of Novel Cardiovascular Biomarkers in Pediatric Patients with Chronic Kidney Disease.Mini reviews in medicinal chemistry · 2024Review
- Lysozyme promotes renal fibrosis through the JAK/STAT3 signal pathway in diabetic nephropathy.Archives of medical science : AMS · 2024Article
- Plasma proteomics analysis of Chinese HIV-1 infected individuals focusing on the immune and inflammatory factors afford insight into the viral control mechanism.Frontiers in immunology · 2024Article
- CXCL6: A potential therapeutic target for inflammation and cancer.Clinical and experimental medicine · 2023Review
- The crosstalk between glomerular endothelial cells and podocytes controls their responses to metabolic stimuli in diabetic nephropathy.Scientific reports · 2023Article
- An invasive zone in human liver cancer identified by Stereo-seq promotes hepatocyte-tumor cell crosstalk, local immunosuppression and tumor progression.Cell research · 2023Article
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Corrections and comments
- Retraction · 2024-12-04Concerns/Issues about Data · Concerns/Issues about Image · Duplication of Data · Duplication of/in Image · Investigation by Journal/Publisher · Investigation by Third Party · Original Data and/or Images not Provided and/or not Available · Unreliable Data · Unreliable Results and/or Conclusions · · See also: https://pubpeer.com/publications/BA743618D3EF58AFDF68D70903D7E1
- Retracted
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study the role of CXCL6 in diabetic nephropathy (DN) was investigated. It was found to be overexpression in DN patients and DN rat model. And the expression of fibrosis-related cytokines was consistent with the expression of CXCL6. High glucose significantly increased the proliferation of rat renal fibroblasts NRK-49F cell and the expression of CXCL6. Knockdown of CXCL6 ameliorated the pro-proliferation effect of high glucose and decreased the expression of fibrosis-related cytokines, while CXCL6 overexpression exhibited the opposite phenomenon. Gene set enrichment analysis, Western blot and ELISA showed that Janus kinase-signal transducer and activator of transcription (JAK-STAT) and CYTOKINE_CYTOKINE_RECEPTOR_INTERACTION signaling pathways were correlative with CXCL6. This data indicates that CXCL6 may promote fibrosis-related factors to accelerate the development of DN renal interstitial fibrosis by activating JAK/STAT3 signaling pathway. CXCL6 is promising to be a potential novel therapeutic target and candidate biomarker for JAK/STAT3 signaling for the treatment of DN.
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