Soluble TWEAK and atheromatosis progression in patients with chronic kidney disease

Fernández‐Laso, Valvanera; Méndez‐Barbero, Nerea; Valdivielso, José M.; Betriu, Àngels; Fernàndez, Elvira; Egido, Jesús; Martı́n-Ventura, José Luis; Blanco-Colio, Luís Miguel

doi:10.1016/j.atherosclerosis.2017.03.043

Cited by 19 publications

(18 citation statements)

References 42 publications

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“…It has been demonstrated that sTWEAK levels are associated with the presence and progression of acute or chronic disease. 19,21,30,31 However, the plausible regulation of sTWEAK levels and Fn14 expression during anaphylaxis is still unknown. By using 2 experimental mouse models that simulate different degrees of allergic sensitivity, we have evaluated circulating sTWEAK concentrations in blood samples and TWEAK expression in lungs.…”

Section: Expression Of Tweak and The Fn14 Receptor Increase In Mouse mentioning

confidence: 99%

“…15,16 TWEAK/Fn14 interaction plays a crucial role in a variety of pathologic inflammatory disorders, such as atherosclerosis, cardiac dysfunction, diabetes, and chronic kidney disease. [17][18][19][20] TWEAK/Fn14 has also been suggested as a potential target to limit edema formation, a major problem in patients with stroke. 21 In addition, it has been suggested that TWEAK/Fn14 signaling is relevant to angiogenesis.…”

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confidence: 99%

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The TNF-like weak inducer of the apoptosis/fibroblast growth factor–inducible molecule 14 axis mediates histamine and platelet-activating factor–induced subcutaneous vascular leakage and anaphylactic shock

Yuste-Montalvo

Nuñez‐Borque

Jensen

et al. 2020

Journal of Allergy and Clinical Immunology

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Background: Anaphylaxis includes mast cell (MC) activation, but less is known about downstream mechanisms (ie, vascular permeability controlled by endothelial cells [ECs]). The TNFlike weak inducer of apoptosis (TWEAK) and its sole receptor, fibroblast growth factor-inducible molecule 14 (Fn14), belong to the TNF superfamily and are involved in proinflammatory responses. Objective: We sought to investigate the role of TWEAK/Fn14 axis in anaphylaxis. Methods: In vivo vascular permeability and mouse models of passive systemic anaphylaxis (PSA) and active systemic anaphylaxis were applied to wild-type (WT), TWEAK-and Fn14-deficient mice (TWEAK 2/2 and Fn14 2/2 , respectively). Primary bone marrow-derived mast cells (BMMCs) and ECs from WT and Fn14 2/2 or TWEAK 2/2 mice were studied. The TWEAK/Fn14 axis was also investigated in human samples. Results: Mice with PSA and active systemic anaphylaxis had increased Fn14 and TWEAK expression in lung tissues and increased serum soluble TWEAK concentrations. TWEAK and Fn14 deficiencies prevent PSA-related symptoms, resulting in resistance to decreased body temperature, less severe reactions, and maintained physical activity. Numbers of MCs after PSA are similar between genotypes in different tissue regions, such as ear skin and the trachea, tongue, peritoneum, lungs, and bone marrow. Moreover, in vitro studies revealed no differences in degranulation or mediator release between WT and Fn14 2/2 BMMCs after IgE-FcεRI stimulation. In vivo and in vitro histamine and platelet-activating factor administration increases Fn14 receptor expression in lungs and ECs. Moreover, Fn14 deficiency in ECs maintained in vitro impermeability when stimulated by mediators or activated BMMCs but not by TWEAK 2/2 BMMCs, indicating that Fn14 is crucial for endothelial barrier function. TWEAK/Fn14 deletion or TWEAK-blocking antibody prevented histamine/plateletactivating factor-induced vascular subcutaneous permeability. Circulating soluble TWEAK levels were increased in patients with anaphylaxis, and plasma from those patients increased Fn14 expression in ECs. Conclusion: The TWEAK/Fn14 axis participates in anaphylactic reactions. Inhibition of TWEAK/Fn14 interaction could be efficacious in anaphylaxis therapy.

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Section: Expression Of Tweak and The Fn14 Receptor Increase In Mouse mentioning

confidence: 99%

mentioning

confidence: 99%

The TNF-like weak inducer of the apoptosis/fibroblast growth factor–inducible molecule 14 axis mediates histamine and platelet-activating factor–induced subcutaneous vascular leakage and anaphylactic shock

Yuste-Montalvo

Nuñez‐Borque

Jensen

et al. 2020

Journal of Allergy and Clinical Immunology

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“…Out of those, 481 had available plasma samples to measure FGF-2 levels. Samples from the other patients had already been spent to measure other biomarkers in sub-studies within the NEFRONA study (22,23). In any case, both populations did not differ in most of the parameters of the study, although there was a lower proportion of patients in dialysis than in the total sample.…”

Section: Design and Study Populationmentioning

confidence: 99%

Association of FGF-2 Concentrations with Atheroma Progression in Chronic Kidney Disease Patients

Božić

Betriu

Bermúdez-López

et al. 2018

CJASN

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“…TWEAK is expressed in several tissues (i.e., heart, brain, and lung) and cells (endothelial and smooth muscle cells). Human studies showed that in patients with chronic kidney disease, sTWEAK was associated with impaired FMD [10,11] and atheromatosis progression [12]. It was also found that in artery samples from patients with atherosclerosis, sTWEAK concentrations were correlated with increased carotid intima-media thickness (c-IMT), a hallmark of subclinical atherosclerotic disease [13].…”

Section: Introductionmentioning

confidence: 99%

Periodontitis and vascular inflammatory biomarkers: an experimental in vivo study in rats

et al. 2019

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The objective of this preclinical in vivo study was to determine changes in vascular inflammatory biomarkers in systemic circulation after injection of lipopolysaccharide (LPS) from Porphyromonas gingivalis (Pg) in rats. Experimental periodontitis was induced by injections of Pg-LPS. Gingival soft and hard tissues changes were analysed by means of magnetic resonance imaging and micro computed tomography. Serum levels of interleukin (IL)-6, IL-10, pentraxin (PTX) 3, and soluble fragment of tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) were determined at baseline and 24 h, 7, 14, and 21 days after periodontal induction. Significant periodontal inflammation and alveolar bone loss were evident at the end of periodontal induction. Experimental periodontitis posed an acute systemic inflammatory response with increased serum levels of IL-6 and PTX3 at 24 h post-induction, followed by a significant overexpression of sTWEAK at 7 days. This inflammatory state was maintained until the end of the experiment (21 days). As expected, IL-10 serum levels were significantly lower during the follow-up compared to baseline concentrations. In the present animal model, experimental periodontitis is associated with increased systemic inflammation. Further studies are needed to confirm whether PTX3 and sTWEAK could be useful biomarkers to investigate potential mechanisms underlying the relationship between periodontitis and atherosclerotic vascular diseases.

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Soluble TWEAK and atheromatosis progression in patients with chronic kidney disease

Abstract: Lower sTWEAK concentrations are associated with atherosclerotic burden and atheromatosis progression in CKD patients free of clinical CVD. These data suggest that sTWEAK could serve as a biomarker to predict CV risk before clinical manifestations.

Cited by 19 publications

References 42 publications

The TNF-like weak inducer of the apoptosis/fibroblast growth factor–inducible molecule 14 axis mediates histamine and platelet-activating factor–induced subcutaneous vascular leakage and anaphylactic shock

The TNF-like weak inducer of the apoptosis/fibroblast growth factor–inducible molecule 14 axis mediates histamine and platelet-activating factor–induced subcutaneous vascular leakage and anaphylactic shock

Association of FGF-2 Concentrations with Atheroma Progression in Chronic Kidney Disease Patients

Periodontitis and vascular inflammatory biomarkers: an experimental in vivo study in rats

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