Alterations of soluble TWEAK and CD163 concentrations in patients with chronic heart failure

Ptaszyńska‐Kopczyńska, Katarzyna; Marcinkiewicz-Siemion, Marta; Lisowska, Anna; Waszkiewicz, Ewa; Witkowski, Marcin; Jasiewicz, Małgorzata; Mikłasz, Paula; Jakim, Piotr; Galar, Bogdan; Musiał, Włodzimierz J.; Kamiński, Karol

doi:10.1016/j.cyto.2016.02.005

Cited by 34 publications

(26 citation statements)

References 29 publications

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“…In support of this, several previous studies have revealed increased serum level of CD163 along with elevated inflammatory cytokines in patients with atrial fibrillation (27) and coronary heart disease (28). In addition, elevated serum CD163 level was also found in patients with chronic heart failure with reduced ejection fraction (29). Hence, the results of the current study are in line with previous findings, suggesting the potential role of increased CD163 expression in doxorubicin-induced cardiotoxicity.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics identification of potential candidate blood indicators for doxorubicin‑induced heart failure

Wan

Xia

et al. 2018

Exp Ther Med

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The care of individual patients requiring anthracyclines remains challenging as uncertainty persists on predictors of cardiotoxicity. The aim of the present study was to identify potential candidate blood indicators of doxorubicin-induced heart failure. The gene expression profiles of GSE40447 and GSE9128 microarray data were downloaded from the Gene Expression Omnibus database to identify differentially expressed genes (DEGs) using the R/Limma package or GEO2R. Functional and pathway enrichment analysis on DEGs were performed using DAVID database. The cardiovascular disease (CVD)-related DEGs were screen out based on the CardioGenBase database. The protein-protein interaction (PPI) network was constructed with STRING database and visualized by using Cytoscape. Then, the CVD-related DEGs were validated by intersection analysis with DEGs in GSE9128. The overlapping DEGs with a consistent expression pattern in GSE40447 and GSE9128 were identified as candidate indicators for doxorubicin-induced heart failure. A total of 516 DEGs potentially associated with doxorubicin-induced heart failure in GSE40447 were identified, which were mainly enriched in the gene ontology terms related to B cells, leukocytes, lymphocyte activation and B cell receptor signaling pathway. Of the DEGs, 42 were screened out as CVD-related DEGs by using CardioGenBase. Seven genes with high connectivity degree were presented in the PPI network. Finally, 5/6 CVD-related DEGs revealed by the intersection analysis were validated by GSE9128 and highlighted as candidate indicators of doxorubicin-induced heart failure: CD163, CD28, SLC25A20, ANPEP and TLR5. Several genes, including the 5 previously mentioned, were proposed as potential candidate blood indicators for doxorubicin-induced heart failure. Further experimental validations are greatly warranted for future clinical application.

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Section: Discussionmentioning

confidence: 99%

Bioinformatics identification of potential candidate blood indicators for doxorubicin‑induced heart failure

Wan

Xia

et al. 2018

Exp Ther Med

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“…Interleukins, as "upstream" biomarkers of inflammation converge on the central TNF signalling pathway, having major influence on atherosclerosis, and consequently on the risk of cardiovascular disease 32 . Another TNF superfamily member -TWEAK -activates the NF-κB (nuclear factor kappa B) and regulates several cell functions such as proliferation, migration, differentiation, cell death, inflammation, angiogenesis, and collagen synthesis of cardiac fibroblasts 33,34,35 . Low TWEAK has been associated with increased risk of death in patients with overt HF 36 and patients with HF and reduced ejection fraction had lower TWEAK levels compared to "controls" 34 .…”

Section: Inflammation and Apoptosis Clustermentioning

confidence: 99%

“…Another TNF superfamily member -TWEAK -activates the NF-κB (nuclear factor kappa B) and regulates several cell functions such as proliferation, migration, differentiation, cell death, inflammation, angiogenesis, and collagen synthesis of cardiac fibroblasts 33,34,35 . Low TWEAK has been associated with increased risk of death in patients with overt HF 36 and patients with HF and reduced ejection fraction had lower TWEAK levels compared to "controls" 34 . The TWEAK-induced proliferation of cardiomyocytes and its immunomodulatory effects may provide basis to these findings 36 .…”

Section: Inflammation and Apoptosis Clustermentioning

confidence: 99%

“…The TWEAK-induced proliferation of cardiomyocytes and its immunomodulatory effects may provide basis to these findings 36 . Apart from binding to its active receptor Fn14, TWEAK can also bind to a scavenger receptor CD163, which was shown to be upregulated in HF, explaining the decreased levels and activity of TWEAK in HF 34 .…”

Section: Inflammation and Apoptosis Clustermentioning

confidence: 99%

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Proteomic Bioprofiles and Mechanistic Pathways of Progression to Heart Failure

Ferreira

Verdonschot

Collier

et al. 2019

Circ: Heart Failure

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Background: Identifying the mechanistic pathways potentially associated with incident HF may provide a basis for novel preventive strategies. Methods and Results:To identify proteomic biomarkers and the potential underlying mechanistic pathways that may be associated with incident HF defined as first hospitalization for HF, a nestedmatched case-control design was used with cases (incident HF) and controls (without HF) selected from 3 cohorts (>20,000 individuals). Controls were matched on cohort, follow-up time, age, and sex.Two independent sample sets (a "discovery" set, with 286 cases and 591 controls and a "replication" set with 276 cases and 280 controls) were used to discover and replicate the findings. 252 circulating proteins in the plasma were studied. Adjusting for the matching variables age, sex, and follow-up time (and correcting for multiplicity of tests), 89 proteins were found to be associated with incident HF in the discovery phase, of which 38 were also associated with incident HF in the replication phase.These 38 proteins pointed to 4 main network clusters underlying incident HF: 1) inflammation and apoptosis, indicated by the expression of the TNF-family members; 2) extracellular matrix remodelling, angiogenesis and growth, indicated by the expression of proteins associated with collagen metabolism, endothelial function and vascular homeostasis; 3) blood pressure regulation, indicated by the expression of natriuretic peptides and proteins related to the renin angiotensin aldosterone system; and 4) metabolism, associated with cholesterol and atherosclerosis.Conclusion: Clusters of biomarkers associated with mechanistic pathways leading to HF were identified linking inflammation, apoptosis, vascular function, matrix remodelling, blood pressure control and metabolism. These findings provide important insight on the pathophysiological mechanisms leading to HF.

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“…Soluble TWEAK forms trimer molecules and acts by binding to its cell surface receptor, fibroblast growth factor‐inducible 14 (Fn14), and their engagement triggers the above‐mentioned functions via activation of several intracellular signaling pathways including the NF‐κB pathway . The amount of TWEAK in the blood was reported to be correlated with the severity of atherosclerosis, diabetes, heart failure, and some autoimmune diseases, suggesting that the changes in the activity of this cytokine are involved in the molecular mechanisms underlying these diseases .…”

Section: Introductionmentioning

confidence: 99%

The C‐terminal region of tumor necrosis factor like weak inducer of apoptosis is required for interaction with advanced glycation end products

Watanabe

Toyomura

Wake

et al. 2018

Biotech and App Biochem

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Previously, we found that endogenously produced pro-inflammatory molecules, advanced glycation end products (AGEs), interact with tumor necrosis factor-like weak inducer of apoptosis (TWEAK), and attenuate its immunomodulatory function. In the present study, to elucidate the mechanism by which AGEs attenuate TWEAK function, we searched for regions responsible for TWEAK-AGE interaction using TWEAK deletion mutants. Pull-down assays with the TWEAK mutants and AGEs revealed that the C-terminal half of TWEAK, which is the region essential for receptor stimulation, was required for this interaction. On the other hand, the N-terminal deletion mutants did not exhibit a significant decrease in AGE binding. Moreover, a moderate decrease in the AGE binding by double-deletion in quartered C-terminal half regions and a substantial decrease by triple-deletion in this region were observed. In addition, full-length TWEAK stimulated IL-8 gene expression in endothelial EA.hy.926 cells, whereas the triple-deletion mutant lost much of this activity, suggesting that the TWEAK-AGE interaction sites overlap with the region needed to exert normal function of TWEAK. Our present findings may help to elucidate the pathophysiological roles of the TWEAK-AGE interaction for prevention and treatment of AGE-related inflammatory diseases. C 2018

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Alterations of soluble TWEAK and CD163 concentrations in patients with chronic heart failure

Cited by 34 publications

References 29 publications

Bioinformatics identification of potential candidate blood indicators for doxorubicin‑induced heart failure

Bioinformatics identification of potential candidate blood indicators for doxorubicin‑induced heart failure

Proteomic Bioprofiles and Mechanistic Pathways of Progression to Heart Failure

The C‐terminal region of tumor necrosis factor like weak inducer of apoptosis is required for interaction with advanced glycation end products

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