Multiple cytokine biomarkers in heart failure

Vistnes, Maria; Christensen, Geir; Omland, Torbjørn

doi:10.1586/erm.10.3

Cited by 21 publications

(14 citation statements)

References 81 publications

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“…Several reports have demonstrated enhanced expression and release of inflammatory cytokines such as TNFα, IL-1, IL-6, IL-18, cardiotrophin-1 (CT-1) and Fas ligand, as well as several chemokines [e.g., monocyte chemoattractant peptide (MCP)-1/CCL2, IL-8/CXCL8, CXCL16 and CCL21 in HF patients [3,4,[7][8][9][10]18,19]. Plasma levels of these molecules appear to be elevated in direct proportion to deterioration of functional class (i.e.…”

Section: Patho-genetic Role Of Inflammation In Hfmentioning

confidence: 99%

“…NYHA classification) and cardiac performance [i.e. left ventricular ejection fraction (LVEF)] [3,4,[7][8][9][10]18,19]. A series of experimental studies have revealed that the biological effects of cytokines may explain several aspects of the syndrome of chronic HF and the pathogenic role of inflammatory cytokines in HF is supported by various transgenic mouse models.…”

Section: Patho-genetic Role Of Inflammation In Hfmentioning

confidence: 99%

“…The finding of elevated levels of tumor necrosis factor (TNF) in sera of HF patients initiated the "inflammation era" in HF research [5]. Since then, a large body of evidence has implicated activation of inflammatory pathways as an important pathological event in the initiation and progression of the syndrome [6][7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

“…In addition to their direct involvement as mediators in the pathogenesis of HF, inflammatory cytokines and related mediators could also be suitable markers for risk stratification and prognostication in HF patients [7][8][9][10]. Numerous reports have suggested that inflammatory cytokines may predict adverse outcome in these patients.…”

Section: Introductionmentioning

confidence: 99%

“…Numerous reports have suggested that inflammatory cytokines may predict adverse outcome in these patients. However, many studies have been limited in sample size and lacking full adjustment with the most recent and strongest biochemical predictors such as NT-proBNP, hs-cTn and C-reactive protein (CRP) [7][8][9][10][17][18][19], which are frequently available as routine tests. Furthermore, a number of pre-analytical and analytical aspects of cytokine measurements may limit their use as biomarkers.…”

Section: Introductionmentioning

confidence: 99%

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Inflammatory cytokines as biomarkers in heart failure

Ueland

Gullestad

Nymo

et al. 2015

Clinica Chimica Acta

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Section: Patho-genetic Role Of Inflammation In Hfmentioning

confidence: 99%

Section: Patho-genetic Role Of Inflammation In Hfmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Inflammatory cytokines as biomarkers in heart failure

Ueland

Gullestad

Nymo

et al. 2015

Clinica Chimica Acta

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Need for a three-focused approach to nonalcoholic fatty liver disease

2011

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We read with interest the reviews by Ghouri et al. 1 and Martinez et al. 2 Ghouri et al. analyzed the association of nonalcoholic fatty liver disease (NAFLD) with cardiovascular disease (CVD) and concluded that although a diagnosis of NAFLD should prompt diabetes screening, it is insufficient for considering patients to be at high risk for CVD. Martinez et al. evaluated noninvasive methods for assessing liver fibrosis and recommended that those tests with the highest diagnostic accuracy be validated against liver biopsy to facilitate their implementation in clinical practice.We meta-analyzed prospective data regarding the natural history of NAFLD and studies assessing the diagnostic accuracy of noninvasive methods for liver disease severity against liver biopsy in NAFLD, and we reached the following conclusions 3 :1. The two NAFLD histological subtypes, simple steatosis (SS) and nonalcoholic steatohepatitis (NASH), have different risks of liver-related complications: SS progresses to cirrhosis in less than 5% of cases; NASH progresses to cirrhosis in 10% to 15% of cases over 10 years and in 25% to 30% of cases in the presence of advanced fibrosis. 2. NAFLD patients have a 1.44-to 2.05-fold higher rate of CVD (depending on whether the diagnosis is based on an aminotransferase elevation or radiological/histological criteria) than the general population; restricting the analysis to studies adjusting for metabolic syndrome did not change the risk. Importantly, CVD mortality did not differ among NAFLD histological subtypes. ; restricting the analysis to studies adjusting for metabolic syndrome did not change the risk. Whether the risk of diabetes differs among NAFLD histological subtypes remains unclear: in a communitybased study, the 13-year incidence of diabetes was 2.98-fold higher in NASH patients versus SS patients. 3According to our analysis, a diagnosis of NAFLD should prompt a thorough three-focus assessment of cardiovascular, metabolic, and liver-related risks (Table 1). 4 Liver-related risk assessment remains problematic because it requires liver histology. Three noninvasive methods have been extensively validated: enzyme-linked immunosorbent assay-detected cytokeratin 18 fragments (9 studies enrolling 856 participants) for the detection of NASH and the NAFLD fibrosis score (13 studies enrolling 3064 participants) and FibroScan (6 studies enrolling 563 participants) for the detection of advanced fibrosis. We believe that these methods should be promptly implemented in diagnostic algorithms to select patients for liver biopsy in routine clinical practice while we continue to search for the ideal noninvasive marker.

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Glycoxydation promotes vascular damage Via MAPK‐ERK/JNK pathways

Nigris¹,

Rienzo²,

Sessa³

et al. 2012

Journal Cellular Physiology

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Oxidation and glycation enhance foam cell formation via MAPK/JNK in euglycemic and diabetic subjects. Here, we investigated the effects of glycated and oxidized LDL (glc-oxLDL) on MAPK-ERK and JNK signaling pathways using human coronary smooth muscle cells. Glc-oxLDL induced a broad cascade of MAPK/JNK-dependent signaling transduction pathways and the AP-1 complex. In glc-oxLDL treated coronary arterioles, tumor necrosis factor (TNF) α increased JNK phosphorylation, whereas protein kinase inhibitor dimethylaminopurine (DMAP) prevented the TNF-induced increase in JNK phosphorylation. The role of MKK4 and JNK were then investigated in vivo, using apolipoprotein E knockout (ApoE(-/-)) mice. Peritoneal macrophages, isolated from spontaneously hyperlipidemic but euglycemic mice showed increases in both proteins and phosphorylated proteins. Compared to streptozotocin-treated diabetic C57BL6 and nondiabetic C57BL6 Wt mice, in streptozotocin-diabetic ApoE(-/-) mice, the increment of foam cell formation corresponded to an increment of phosphorylation of JNK1, JNK2, and MMK4. Thus, we provide a first line of evidence that MAPK-ERK/JNK pathways are involved in vascular damage induced by glycoxidation.

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Multiple cytokine biomarkers in heart failure

Cited by 21 publications

References 81 publications

Inflammatory cytokines as biomarkers in heart failure

Inflammatory cytokines as biomarkers in heart failure

Need for a three-focused approach to nonalcoholic fatty liver disease

Glycoxydation promotes vascular damage Via MAPK‐ERK/JNK pathways

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