Divergent Tumor Necrosis Factor Receptor–Related Remodeling Responses in Heart Failure

Abstract Background and Aims The “Shrunken pore syndrome” is characterized by a difference in renal filtration between cystatin C and creatinine resulting in a low eGFRcystatinC/eGFRcreatinine-ratio, and studies have demonstrated a high risk for cardiovascular morbidity and mortality for patients with shrunken pore syndrome. In this observational study, we explored associations between shrunken pore syndrome and proteins implicated in cardiovascular disease and inflammation in patients with heart failure. Method Plasma samples from 300 individuals HARVEST-Malmö trial hospitalized for the diagnosis of heart failure (mean age 75 years; 30% female), were analyzed with a proximity extension assay consisting of 92 proteins, to identify proteins associated with shrunken pore syndrome. Shrunken pore syndrome was defined as eGFRcystatinC ≤60% of eGFRcreatinine. Proteins associated with shrunken pore syndrome in the initial age and sex-adjusted analyses (Bonferroni-corrected p≤ 5.4x10-4) were further adjusted for relevant covariates. Results In multivariate analyses, Shrunken pore syndrome was associated with elevated levels of six proteins; scavenger receptor cysteine-rich type 1 protein M130, tumor necrosis factor receptor 1, tumor necrosis factor receptor 2, osteoprotegerin, interleukin-2 receptor subunit alpha, and tyrosine-protein kinase receptor UFO (p<0.05). Conclusion In heart failure patients, shrunken pore syndrome was independently associated with proteins linked to atherosclerosis and cell proliferation.

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Soluble tumor necrosis factor receptor levels identify a subgroup of heart failure patients with increased cardiomyocyte apoptosis

Clinica Chimica Acta ◽

10.1016/s0009-8981(02)00058-x ◽

2002 ◽

Vol 320 (1-2) ◽

pp. 65-67 ◽

Cited By ~ 9

Author(s):

Antti Saraste ◽

Liisa-Maria Voipio-Pulkki ◽

Päivi Heikkilä ◽

Petri Laine ◽

Markku S Nieminen ◽

...

Keyword(s):

Heart Failure ◽

Tumor Necrosis Factor ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Receptor ◽

Cardiomyocyte Apoptosis ◽

Heart Failure Patients ◽

Necrosis Factor

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Soluble Tumor Necrosis Factor Receptor Type I and Granulysin as Immunological Markers in Congestive Heart Failure

American Journal of Immunology ◽

10.3844/ajisp.2005.119.124 ◽

2005 ◽

Vol 1 (3) ◽

pp. 119-124

Author(s):

Simone de Lima e Sil Deo ◽

Maria do Carmo Valen Crasto ◽

Alda Maria Da-Cruz ◽

Milton OzÃ³rio Moraes ◽

Alexandre Pio Abreu ◽

...

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Tumor Necrosis Factor ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Receptor ◽

Receptor Type ◽

Type I ◽

Immunological Markers ◽

Necrosis Factor

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Identification of Genetic Variants of the Tumor Necrosis Factor Receptor 2 Gene (TNFRSF1B) in Patients with Heart Failure

Journal of Cardiac Failure ◽

10.1016/j.cardfail.2007.06.403 ◽

2007 ◽

Vol 13 (6) ◽

pp. S101-S102

Author(s):

Akash Makkar ◽

Javier Banchs ◽

Mary A. Hauck ◽

Tariq S. Siddiqui ◽

Saeed A. Jortani ◽

...

Keyword(s):

Heart Failure ◽

Tumor Necrosis Factor ◽

Genetic Variants ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Receptor ◽

Patients With Heart Failure ◽

Necrosis Factor

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Association among Soluble Tumor Necrosis Factor Receptor I, Matrix Metalloproteinase-9, Procollagen C-terminal Propeptide type I, and N-Terminal proBrain Natriuretic Peptide in Heart Failure

The Indonesian Biomedical Journal ◽

10.18585/inabj.v3i1.136 ◽

2011 ◽

Vol 3 (1) ◽

pp. 64

Author(s):

Mona Yolanda ◽

Marsetio Donosepoetro ◽

Anwar Santoso ◽

Mansyur Arif

Keyword(s):

Heart Failure ◽

Tumor Necrosis Factor ◽

Linear Regression ◽

Path Analysis ◽

Linear Model ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Receptor ◽

General Linear Model ◽

General Linear ◽

Necrosis Factor

BACKGROUND: Heart failure (HF) is associated with an increased expression of proinflammatory cytokines, especially soluble tumor necrosis factor receptor I (sTNFR I), but the underlying mechanism to the relationship between sTNFR I activation and the progression of HF is not yet fully understood. This study aims to see the association between sTNFR I, MMP-9, PICP, and NT-proBNP in the progression of HF.METHODS: This was a cross sectional study which recruited 45 subjects with HF confirmed by echocardiography and NT-proBNP. Concentration sTNFR I, MMP-9, and PICP were measured using ELISA method, whereas NT-proBNP concentration was measured using ECLIA method. Univariate linear regression analysis, path analysis and General Linear Model were used to determine which parameters played the most significant role in HF.RESULTS: Results of the univariate linear regression and path analysis showed there was a linear relationship between sTNFR I with MMP-9, with R square of 25.8% (p=0.00; r=0.508), R square sTNFRI and MMP-9 with PICP was 14.4% (p=0.038; r=0.379) and R square MMP-9 and PICP with NT-proBNP was 39.6% (p=0.00; r=0.629). From the General Linear Model we found that the important predictor for HF was through MMP-9 and PICP.CONCLUSION: sTNFR I as a proinflammatory factor is one of the factors involved in the heart failure as seen by NT-proBNP through activation of brosis (PICP) and remodeling factor (MMP-9).KEYWORDS: sTNFR I, MMP-9, PICP, NT-proBNP, heart failure

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Plasma Soluble Tumor Necrosis Factor Receptor Concentrations and Clinical Events after Hospitalization: Findings from ASSESS-AKI and ARID studies

10.1101/2021.11.08.21266015 ◽

2021 ◽

Author(s):

Steven G. Coca ◽

George Vasquez-Rios ◽

Sherry Mansour ◽

Dennis G. Moledina ◽

Heather Thiessen-Philbrook ◽

...

Keyword(s):

Heart Failure ◽

Acute Kidney Injury ◽

Tumor Necrosis Factor ◽

Kidney Disease ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Receptor ◽

Kidney Injury ◽

Clinical Events ◽

Necrosis Factor

Background: The role of plasma soluble tumor necrosis factor receptor (sTNFR)1 and sTNFR2 in the prognosis of clinical events after hospitalization with or without acute kidney injury (AKI) is unknown. Methods: We measured sTNFR1 and sTNFR2 obtained 3 months post-discharge using samples from Assessment, Serial Evaluation, and Subsequent Sequelae of Acute Kidney Injury (ASSESS-AKI) and AKI Risk in Derby (ARID) that enrolled patients with and without AKI. The associations between biomarkers with longitudinal kidney disease incidence and progression, heart failure, and death were evaluated. Analyses were adjusted for demographics and key covariates at the 3-month visit. Results: Among 1474 participants with plasma biomarker measurements, 19% developed kidney disease progression, 14% had later heart failure, and 21% died over a median follow-up of 4.4 years. For the kidney outcome, the adjusted HRs per doubling in concentration were 2.9 (2.2-3.9) for sTNFR1 and 1.9 (1.5-2.5) for sTNFR2. AKI during the index hospitalization did not modify the association between biomarkers and kidney events. For heart failure, the adjusted HRs per doubling in concentration were 1.9 (1.4-2.5) for sTNFR1 and 1.5 (1.2-2.0) for sTNFR2. For mortality, the adjusted HRs were 3.3 (2.5-4.3) for sTNFR1 and 2.5 (2.0-3.1) for sTNFR2. The findings in ARID were qualitatively similar for the magnitude of association between biomarkers and outcomes. Conclusion: Plasma sTNFR1 and sTNFR2 measured 3 months after discharge were independently associated with clinical events, regardless of AKI status during the index admission. sTNFR1 and sTNFR2 may assist with the risk stratification of patients during follow-up.

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