Impact of soluble TWEAK and CD163/TWEAK ratio on long-term cardiovascular mortality in patients with peripheral arterial disease

Urbonavičienė, Gražina; Martin-Ventura, José Luis; Lindholt, Jes Sanddal; Urbonavičius, Sigitas; Moreno, Juan Antonio; Egido, Jesús; Blanco-Colio, Luís Miguel

doi:10.1016/j.atherosclerosis.2011.09.016

Cited by 54 publications

(58 citation statements)

References 32 publications

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“…Accordingly, the sCD163/sTWEAK ratio may act as an indicator of atherothrombosis progression (91). Similar results were revealed in other atherosclerotic related diseases such as coronary artery disease with or without chronic kidney disease (19,20,58). It seems counterfactual that, as an inflammatory factor, sTWEAK concentration decreased in these atherosclerotic related diseases (19,20,58).…”

Section: Cd163 and Tweaksupporting

confidence: 52%

“…CD163 is a marker for anti-inflammatory activity in macrophages (57) and is potentially a newly identified receptor for TWEAK, as reported previously (18,21). Increasing in vivo and in vitro evidence suggests that the interaction between TWEAK and CD163 may affect the development of atherosclerosis and related diseases (19,20,(57)(58)(59)(60).…”

Section: Cd163: the Second Definite Receptormentioning

confidence: 66%

“…Additionally, the TWEAK/Fn14 combination may become a novel target of interference in atherosclerosis development. As for CD163, in addition to its potential diagnostic uses in atherosclerosis-related diseases, it is also an interesting candidate for medical therapy (19,57,58,60). This is because CD163, as an example of the atheroprotective intraplaque population, eliminates free-Hb and releases a large quantity of anti-inflammatory mediators via activating downstream pathways (62,64).…”

Section: Therapeutic Considerationsmentioning

confidence: 99%

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The role of tumor necrosis factor-like weak inducer of apoptosis in atherosclerosis via its two different receptors

Liu

Lin

Xiang

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. At present, it is commonly accepted that atherosclerosis is a chronic inflammatory disease characterized by disorder of the arterial wall. As one of the inflammatory cytokines of the tumor necrosis factor superfamily, tumor necrosis factor-like weak inducer of apoptosis (TWEAK) participates in the formation and progression of atherosclerosis. TWEAK, when binding to its initial receptor, fibroblast growth factor inducible molecule 14 (Fn14), exerts adverse biological functions in atherosclerosis, including dysfunction of endothelial cells, phenotypic change of smooth muscle cells and inflammatory responses of monocytes/macrophages. However, accumulating data supports that, besides Fn14, TWEAK also binds to cluster of differentiation (CD)163, an anti-inflammatory cytokine and a scavenger receptor exclusively expressed by monocytes and macrophages. Furthermore, it has been demonstrated that CD163 is able to internalize TWEAK and likely elicits protective effects in atherosclerosis by terminating inflammation induced by TWEAK. In the present study, the role of TWEAK in atherosclerosis was reviewed, with a predominant focus on CD163 and Fn14 receptors.

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Section: Cd163 and Tweaksupporting

confidence: 52%

Section: Cd163: the Second Definite Receptormentioning

confidence: 66%

Section: Therapeutic Considerationsmentioning

confidence: 99%

See 1 more Smart Citation

The role of tumor necrosis factor-like weak inducer of apoptosis in atherosclerosis via its two different receptors

Liu

Lin

Xiang

et al. 2017

Experimental and Therapeutic Medicine

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“…TWEAK enhances proliferation of endothelial cells and induces tissue factor and plasminogen activator inhibitor 1 in atherosclerotic plaques, and, indeed, pharmacological inhibition of TWEAK with TWEAK-specific Abs or Fn14-Fc reduces vascular damage in the ApoE knockout model of atherosclerosis (44)(45)(46). Furthermore, concentrations of soluble TWEAK have been found to be reduced in samples of patients suffering arterial hypertension (47), atherosclerosis (48), or abdominal aortic aneurysm (49) and are of poor prognosis in patients with ischemic heart failure (50, 51) and artery disease (52). Collectively, these data give clear evidence that the TWEAK-Fn14 system is of relevance for atherosclerosis and heart failure-associated pathologies.…”

Section: Discussionmentioning

confidence: 99%

TWEAK Inhibits TRAF2-Mediated CD40 Signaling by Destabilization of CD40 Signaling Complexes

Salzmann

Lang

Rosenthal

et al. 2013

The Journal of Immunology

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We found recently that TNF-like weak inducer of apoptosis (TWEAK) and fibroblast growth factor–inducible-14 (Fn14) by virtue of their strong capability to reduce the freely available cytoplasmic pool of TNFR-associated factor (TRAF)2 and cellular inhibitors of apoptosis (cIAPs) antagonize the functions of these molecules in TNFR1 signaling, resulting in sensitization for apoptosis and inhibition of classical NF-κB signaling. In this study, we demonstrate that priming of cells with TWEAK also interferes with activation of the classical NF-κB pathway by CD40. Likewise, there was strong inhibition of CD40 ligand (CD40L)–induced activation of MAPKs in TWEAK-primed cells. FACS analysis and CD40L binding studies revealed unchanged CD40 expression and normal CD40L–CD40 interaction in TWEAK-primed cells. CD40L immunoprecipitates, however, showed severely reduced amounts of CD40 and CD40-associated proteins, indicating impaired formation or reduced stability of CD40L–CD40 signaling complexes. The previously described inhibitory effect of TWEAK on TNFR1 signaling has been traced back to reduced activity of the TNFR1-associated TRAF2–cIAP1/2 ubiquitinase complex and did not affect the stability of the immunoprecipitable TNFR1 receptor complex. Thus, the inhibitory effect of TWEAK on CD40 signaling must be based at least partly on other mechanisms. In line with this, signaling by the CD40-related TRAF2-interacting receptor TNFR2 was also attenuated but still immunoprecipitable in TWEAK-primed cells. Collectively, we show that Fn14 activation by soluble TWEAK impairs CD40L–CD40 signaling complex formation and inhibits CD40 signaling and thus identify the Fn14-TWEAK system as a potential novel regulator of CD40-related cellular functions.

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“…It has therefore been considered a pro-inflammatory biomarker of several cardiovascular diseases, including insulin resistance and T2D [22]. Along the same lines, the demonstration of systemic M1 polarisation in patients with OSA related to nocturnal hypoxia intensity could contrast with the previous description of M2 polarisation in animal models with tumour infiltration subjected to intermittent hypoxia [23].…”

mentioning

confidence: 99%

Sleep apnoea, insulin resistance and diabetes: the first step is in the fat

Almendros

García‐Río

2017

Eur Respir J

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Impact of soluble TWEAK and CD163/TWEAK ratio on long-term cardiovascular mortality in patients with peripheral arterial disease

Cited by 54 publications

References 32 publications

The role of tumor necrosis factor-like weak inducer of apoptosis in atherosclerosis via its two different receptors

The role of tumor necrosis factor-like weak inducer of apoptosis in atherosclerosis via its two different receptors

TWEAK Inhibits TRAF2-Mediated CD40 Signaling by Destabilization of CD40 Signaling Complexes

Sleep apnoea, insulin resistance and diabetes: the first step is in the fat

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