CXCL16 in kidney and cardiovascular injury

Izquierdo, María C.; Martín-Cleary, Catalina; Fernández-Fernández, Beatriz; Elewa, Usama; Sanchez-Niño, María Dolores; Carrero, Juan Jesús; Ortíz, Alberto

doi:10.1016/j.cytogfr.2014.04.002

Cited by 60 publications

(51 citation statements)

References 82 publications

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“…Moreover, previous data have also suggested that there is a role for CXCL16 in promoting myocardial fibroblast proliferation and increasing matrix metalloproteinase activity in cardiomyocytes and myocardial fibroblasts [4]. These functions imply a pathogenic role for CXCL16 in cardiovascular diseases (CVD), and this notion is supported by various animal studies that have been summarized in a review by Izquierdo et al [5]. …”

Section: Introductionsupporting

confidence: 55%

Interaction of Soluble CXC Ligand 16 and Cardiac Injury Markers in Hemodialysis Patients

Liu

Wang²,

Wei³

et al. 2017

Am J Nephrol

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Background: Recent data suggest that there is a pathogenic role for CXC ligand 16 (CXCL16) in cardiovascular diseases. Little is known about circulating CXCL16 in patients with kidney dysfunction. We explored the relationships of plasma CXCL16 with cardiac injury markers in a group of dialysis patients. Methods: Plasma CXCL16 and C-reactive protein (CRP) were measured in 366 patients who were on maintenance hemodialysis. Cardiac injury was evaluated via measurements of the circulating B-type natriuretic peptide (BNP), N-terminal prohormone of brain natriuretic peptide (NT proBNP), Troponin I (TnI), and Troponin T (TnT). Sixty healthy subjects who were frequency matched with the patients on the basis of age and gender were recruited as healthy controls. Results: The mean age of the patients was 52.5 ± 12.1 years and 56.3% were male. Circulating CXCL16 was significantly higher in the patients than in the controls (patients vs. controls: 477.3 (367.0-647.1) pg/mL vs. 229.5 (203.8-254.5) pg/mL; p < 0.001). The log-transformed (log-) CXCL16 level was correlated with all 4 cardiac markers (log-BNP, log-NTproBNP, log-TnI, and log-TnT) with high levels of significance (all p < 0.001), even after extensive controls for the covariates. In contrast, CRP was correlated only with BNP (marginally) and NT proBNP and was not correlated with troponins. Conclusion: We showed, for the first time, highly significant relationships of circulating CXCL16 level with cardiac injury markers in dialysis patients. Our data suggest that circulating CXCL16 is possibly involved in the pathological process of cardiovascular damage in dialysis patients and may serve as a therapeutic target for cardiac protection in these patients.

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Section: Introductionsupporting

confidence: 55%

Interaction of Soluble CXC Ligand 16 and Cardiac Injury Markers in Hemodialysis Patients

Liu

Wang²,

Wei³

et al. 2017

Am J Nephrol

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“…This observational study can only be hypothesis generating. The clinical implications will depend on which hypothesis is correct, but may even include circulating CXCL16 being a target for therapy if experimental interventional studies confirm data suggesting a pathogenic role for CXL16 in kidney injury [5]. In this regard, several hypotheses may explain the relationship between parameters of kidney function and plasma CXCL16.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, the kidney may be source of circulating CXCL16 in proteinuric nephropathies, especially if advanced to the point where GFR is decreased. Finally, there is experimental evidence that CXCL16 may cause glomerular injury, adding a further potential explanation between the observed association between circulating CXCL16 and markers of severity of kidney injury [5]. In this regard, CXCL16 is the main scavenger receptor for ox-LDL in human podocytes [30,31].…”

Section: Discussionmentioning

confidence: 99%

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Circulating CXCL16 in Diabetic Kidney Disease

Elewa

Sanchez-Niño

Mahíllo‐Fernández

et al. 2016

Kidney Blood Press Res

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Background/Aims: Chronic kidney disease and, specifically, diabetic kidney disease, is among the fastest increasing causes of death worldwide. A better understanding of the factors contributing to the high mortality may help design novel monitoring and therapeutic approaches. CXCL16 is both a cholesterol receptor and a chemokine with a potential role in vascular injury and inflammation. We aimed at identifying predictors of circulating CXCL16 levels in diabetic patients with chronic kidney disease. Methods: We have now studied plasma CXCL16 in 134 European patients with diabetic kidney disease with estimated glomerular filtration rate (eGFR) categories G1-G4 and albuminuria categories A1-A3, in order to identify factors influencing plasma CXCL16 in this population. Results: Plasma CXCL16 levels were 4.0±0.9 ng/ml. Plasma CXCL16 increased with increasing eGFR category from G1 to G4 (that is, with decreasing eGFR values) and with increasing albuminuria category. Plasma CXCL16 was higher in patients with prior cardiovascular disease (4.33±1.03 vs 3.88±0.86 ng/ml; p=0.013). In multivariate analysis, eGFR and serum albumin had an independent and significant negative correlation with plasma CXCL16. Conclusion: In diabetic kidney disease patients, GFR and serum albumin independently predicted plasma CXCL16 levels.

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“…The membranebound cell surface-expressed form of CXCL16 is a scavenger receptor and adhesion molecule. The cleaved and soluble ectodomain of CXCL16 acts as a proinflammatory chemokine [237]. Activation of P2X7Rs induced the rapid shedding of CXCL16 from RPMI 8226 human myeloma cells involving the metalloprotease a disintegrin and metalloproteinase 10 (ADAM10) [176].…”

Section: Shedding Of Membrane-bound Proteinsmentioning

confidence: 99%

Extracellular ATP and other nucleotides—ubiquitous triggers of intercellular messenger release

Zimmermann

2015

Purinergic Signalling

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Extracellular nucleotides, and ATP in particular, are cellular signal substances involved in the control of numerous (patho)physiological mechanisms. They provoke nucleotide receptor-mediated mechanisms in select target cells. But nucleotides can considerably expand their range of action. They function as primary messengers in intercellular communication by stimulating the release of other extracellular messenger substances. These in turn activate additional cellular mechanisms through their own receptors. While this applies also to other extracellular messengers, its omnipresence in the vertebrate organism is an outstanding feature of nucleotide signaling. Intercellular messenger substances released by nucleotides include neurotransmitters, hormones, growth factors, a considerable variety of other proteins including enzymes, numerous cytokines, lipid mediators, nitric oxide, and reactive oxygen species. Moreover, nucleotides activate or co-activate growth factor receptors. In the case of hormone release, the initially paracrine or autocrine nucleotide-mediated signal spreads through to the entire organism. The examples highlighted in this commentary suggest that acting as ubiquitous triggers of intercellular messenger release is one of the major functional roles of extracellular nucleotides. While initiation of messenger release by nucleotides has been unraveled in many contexts, it may have been overlooked in others. It can be anticipated that additional nucleotide-driven messenger functions will be uncovered with relevance for both understanding physiology and development of therapy.

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CXCL16 in kidney and cardiovascular injury

Cited by 60 publications

References 82 publications

Interaction of Soluble CXC Ligand 16 and Cardiac Injury Markers in Hemodialysis Patients

Interaction of Soluble CXC Ligand 16 and Cardiac Injury Markers in Hemodialysis Patients

Circulating CXCL16 in Diabetic Kidney Disease

Extracellular ATP and other nucleotides—ubiquitous triggers of intercellular messenger release

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