ArticleScientific reports2020
Disruption of CXCR6 Ameliorates Kidney Inflammation and Fibrosis in Deoxycorticosterone Acetate/Salt Hypertension.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- T-Cell Remodeling in Renal Fibrosis: From Acute Injury to Chronic Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- CXCR6+ T cells promote apoptosis and necroptosis in proximal tubules during AKI-to-CKD transition.Cell death & disease · 2026Article
- Mechanisms and Prevention Strategies of Macrophage Involvement in the Progression From Hypertension to Heart Failure.International journal of hypertension · 2025Review
- The multifaceted role of macrophages in kidney physiology and diseases.Frontiers in immunology · 2025Review
- CXC chemokine receptor 7 ameliorates renal fibrosis by inhibiting β-catenin signaling and epithelial-to-mesenchymal transition in tubular epithelial cells.Renal failure · 2024Article
- Association between circulatory complement activation and hypertensive renal damage: a case-control study.Renal failure · 2024Article
- Spatial transcriptomics defines injury specific microenvironments and cellular interactions in kidney regeneration and disease.Nature communications · 2024Article
- Spatial transcriptomics defines injury-specific microenvironments in the adult mouse kidney and novel cellular interactions in regeneration and disease.bioRxiv : the preprint server for biology · 2023Article
- The potential role of complement alternative pathway activation in hypertensive renal damage.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Article
- Myeloid PTEN deficiency aggravates renal inflammation and fibrosis in angiotensin II-induced hypertension.Journal of cellular physiology · 2022Article
- Article
- Further comment on articles pertaining to: "Homocysteine as a potential predictor of cardiovascular risk in patients with COVID-19".Medical hypotheses · 2021Article
- [High-salt exposure induces macrophage polarization to promote proliferation and phenotypic transformation of co-cultured renal fibroblasts].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Circulating cells have a pathogenic role in the development of hypertensive nephropathy. However, how these cells infiltrate into the kidney are not fully elucidated. In this study, we investigated the role of CXCR6 in deoxycorticosterone acetate (DOCA)/salt-induced inflammation and fibrosis of the kidney. Following uninephrectomy, wild-type and CXCR6 knockout mice were treated with DOCA/salt for 3 weeks. Blood pressure was similar between wild-type and CXCR6 knockout mice at baseline and after treatment with DOCA/salt. Wild-type mice develop significant kidney injury, proteinuria, and kidney fibrosis after three weeks of DOCA/salt treatment. CXCR6 deficiency ameliorated kidney injury, proteinuria, and kidney fibrosis following treatment with DOCA/salt. Moreover, CXCR6 deficiency inhibited accumulation of bone marrow-derived fibroblasts and myofibroblasts in the kidney following treatment with DOCA/salt. Furthermore, CXCR6 deficiency markedly reduced the number of macrophages and T cells in the kidney after DOCA/salt treatment. In summary, our results identify a critical role of CXCR6 in the development of inflammation and fibrosis of the kidney in salt-sensitive hypertension.
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