CXCL16 Deficiency Attenuates Renal Injury and Fibrosis in Salt-Sensitive Hypertension

Liu, Hua; Ma, Zhiheng; Peng, Hui; He, Liqun; Hu, Zhaoyong; Wang, Yanlin

doi:10.1038/srep28715

Cited by 36 publications

(30 citation statements)

References 47 publications

(87 reference statements)

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“…Renal expression of CXCL16 is upregulated in Ang II-induced and DOCA-salt hypertension (67, 68). In both hypertensive models, CXCL16-deficient mice have similar blood pressure to wild-type controls.…”

Section: Chemokinesmentioning

confidence: 99%

The role of chemokines in hypertension and consequent target organ damage

Rudemiller

Crowley

2017

Pharmacological Research

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Immune cells infiltrate the kidney, vasculature, and central nervous system during hypertension, consequently amplifying tissue damage and/or blood pressure elevation. Mononuclear cell motility depends partly on chemokines, which are small cytokines that guide cells through an increasing concentration gradient via ligation of their receptors. Tissue expression of several chemokines is elevated in clinical and experimental hypertension. Likewise, immune cells have enhanced chemokine receptor expression during hypertension, driving immune cell infiltration and inappropriate inflammation in cardiovascular control centers. T lymphocytes and monocytes/macrophages are pivotal mediators of hypertensive inflammation, and these cells migrate in response to several chemokines. As powerful drivers of diapedesis, the chemokines CCL2 and CCL5 have long been implicated in hypertension, but experimental data highlight divergent, context-specific effects of these chemokines on blood pressure and tissue injury. Several other chemokines, particularly those of the CXC family, contribute to blood pressure elevation and target organ damage. Given the significant interplay and chemotactic redundancy among chemokines during disease, future work must not only describe the actions of individual chemokines in hypertension, but also characterize how manipulating a single chemokine modulates the expression and/or function of other chemokines and their cognate receptors. This information will facilitate the design of precise chemotactic immunotherapies to limit cardiovascular and renal morbidity in hypertensive patients.

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Section: Chemokinesmentioning

confidence: 99%

The role of chemokines in hypertension and consequent target organ damage

Rudemiller

Crowley

2017

Pharmacological Research

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“…These results suggest that CXCR6 plays a critical role in the development of DOCA/salt-induced hypertensive nephropathy by mediating the recruitment of myeloid fibroblasts and inflammatory cells into the kidney. www.nature.com/scientificreports www.nature.com/scientificreports/ Recently, we have demonstrated that CXCL16 recruits myeloid fibroblasts, macrophages and T lymphocytes into the kidney resulting in kidney injury and fibrosis in a DOCA/salt model of hypertension 9 . CXCL16 regulates circulating cell trafficking via interaction with its receptor CXCR6 16 .…”

Section: Discussionmentioning

confidence: 99%

“…Inflammatory and immune cells are recruited into the kidney by chemokines through interacting with their respective receptors 6,26,32 . Recently, we have demonstrated that genetic deletion of CXCL16 suppresses inflammatory and immune cell infiltration into the kidney following DOCA/salt-induced hypertension 9 . In the present study, we report that the infiltration of macrophage and T lymphocytes into the kidney is dramatically reduced in CXCR6 deficient mice treated with DOCA/salt.…”

Section: Discussionmentioning

confidence: 99%

“…Chemokine (C-X-C motif) ligand 16 (CXCL16) belongs to the CXC chemokine subfamily 8 . We have recently demonstrated that CXCL16 is upregulated in the kidney following deoxycorticosterone acetate (DOCA)/salt administration and genetic deletion of CXCL16 attenuates kidney injury and fibrosis in experimental model of DOCA/salt hypertension 9 . The receptor for CXCL16 is CXCR6, which is expressed on T cells, macrophages, and fibrocytes [10][11][12] .…”

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confidence: 99%

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Disruption of CXCR6 Ameliorates Kidney Inflammation and Fibrosis in Deoxycorticosterone Acetate/Salt Hypertension

Jin

et al. 2020

Sci Rep

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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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“…Genetic deletion of CXCL16 protects the kidney from renal dysfunction, inhibits renal fibrosis, reduces proteinuria, suppresses bone marrow-derived fibroblast accumulation, myofibroblast formation, macrophage and T cell infiltration and pro-inflammatory cytokine expression with no effect on Ang II-induced hypertension 30 . More recently, we have shown that CXCL16 plays a crucial role in the development of kidney fibrosis induced by DOCA/salt and renal artery stenosis 31, 32 .…”

Section: Introductionmentioning

confidence: 99%

Recent Advances in Magnetic Resonance Imaging Assessment of Renal Fibrosis

Kang

et al. 2017

Advances in Chronic Kidney Disease

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Chronic kidney disease is a global public health problem. Renal fibrosis is a final common pathway leading to progressive loss of function in chronic kidney disease. The degree of renal fibrosis predicts the prognosis of chronic kidney disease. Recent studies have shown that bone marrow–derived fibroblasts contribute significantly to the development of renal fibrosis, which may yield novel therapeutic strategy for fibrotic kidney disease. Therefore, it is imperative to accurately assess the degree of renal fibrosis non-invasively to identify those patients who can benefit from anti-fibrotic therapy. In this review, we summarize recent advances in the assessment of renal fibrosis by magnetic resonance imaging.

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CXCL16 Deficiency Attenuates Renal Injury and Fibrosis in Salt-Sensitive Hypertension

Cited by 36 publications

References 47 publications

The role of chemokines in hypertension and consequent target organ damage

The role of chemokines in hypertension and consequent target organ damage

Disruption of CXCR6 Ameliorates Kidney Inflammation and Fibrosis in Deoxycorticosterone Acetate/Salt Hypertension

Recent Advances in Magnetic Resonance Imaging Assessment of Renal Fibrosis

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