Long-Term Survival and Apolipoprotein A1 Level in Chronic Heart Failure: Interaction With Tumor Necrosis Factor α −308 G/A Polymorphism

Gombos, Tímea; Förhécz, Zsolt; Pozsonyi, Zoltán; Jánoskúti, Lívia; Prohászka, Zoltán; Karádi, István

doi:10.1016/j.cardfail.2016.06.004

Cited by 20 publications

(21 citation statements)

References 25 publications

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“…The phenomenon of reduced LDL-C levels has already been described in other chronic diseases such as rheumatoid arthritis 12 , cancer 20 , end-stage renal failure 11 or chronic heart failure 21 however, to the best of our knowledge this is the first study reporting changes in LDL-C levels and their prognostic role in PAH patients. Potential explanations for these findings include a chronic inflammatory state 22 , malnutrition 18 , and altered liver metabolism 17 .…”

Section: Discussionmentioning

confidence: 72%

Low-density lipoprotein cholesterol and survival in pulmonary arterial hypertension

Kopeć

Waligóra

Tyrka

et al. 2017

Sci Rep

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Low-density lipoprotein cholesterol(LDL-C) is a well established metabolic marker of cardiovascular risk, however, its role in pulmonary arterial hypertension (PAH) has not been determined. Therefore we assessed whether LDL-C levels are altered in PAH patients, if they are associated with survival in this group and whether pulmonary hypertension (PH) reversal can influence LDL-C levels. Consecutive 46 PAH males and 94 females were age matched with a representative sample of 1168 males and 1245 females, respectively. Cox regression models were used to assess the association between LDL-C and mortality. The effect of PH reversal on LDL-C levels was assessed in 34 patients with chronic thromboembolic pulmonary hypertension (CTEPH) undergoing invasive treatment. LDL-C was lower in both PAH (2.6 ± 0.8 mmol/l) and CTEPH (2.7 ± 0.7 mmol/l) patients when compared to controls (3.2 ± 1.1 mmol/l, p < 0.001). In PAH patients lower LDL-C significantly predicted death (HR:0.44/1 mmol/l, 95%CI:0.26–0.74, p = 0.002) after a median follow-up time of 33(21–36) months. In the CTEPH group, LDL-C increased (from 2.6[2.1–3.2] to 4.0[2.8–4.9]mmol/l, p = 0.01) in patients with PH reversal but remained unchanged in other patients (2.4[2.2–2.7] vs 2.3[2.1–2.5]mmol/l, p = 0.51). We concluded that LDL-C level is low in patients with PAH and is associated with an increased risk of death. Reversal of PH increases LDL-C levels.

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Section: Discussionmentioning

confidence: 72%

Low-density lipoprotein cholesterol and survival in pulmonary arterial hypertension

Kopeć

Waligóra

Tyrka

et al. 2017

Sci Rep

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“…Experiments show that expression of FAP (fibroblast activation protein alpha) [ 75 ], THBS4 [ 76 ], CD27 [ 77 ], LEF1 [ 78 ], CTHRC1 [ 79 ], ESR1 [ 80 ], CXCL9 [ 81 ], SERPINA3 [ 82 ], TRPC4 [ 83 ], F13A1 [ 84 ], PIK3C2A [ 85 ], KCNIP2 [ 86 ] and GPR4 [ 87 ] contributed to myocardial infarction. MFAP4 [ 88 ], ALOX15 [ 89 ], COL1A1 [ 90 ], APOA1 [ 91 ], PDE5A [ 92 ], CX3CR1 [ 93 ], THY1 [ 94 ], GREM1 [ 95 ], FMOD (fibromodulin) [ 96 ], NPPA (natriuretic peptide A) [ 97 ], LTBP2 [ 98 ], LUM (lumican) [ 99 ], IL34 [ 100 ], NRG1 [ 101 ], CXCL14 [ 102 ], CXCL10 [ 103 ], ACE (angiotensin I converting enzyme) [ 104 ], CFTR (ystic fibrosis transmembrane conductance regulator) [ 105 ], S100A8 [ 106 ], S100A9 [ 106 ], HP (haptoglobin) [ 107 ], AGTR1 [ 108 ], ATP2A2 [ 109 ], IL10 [ 110 ], EDN1 [ 111 ], TLR2 [ 112 ], MCEMP1 [ 113 ], TPO (thyroid peroxidase) [ 114 ], CD163 [ 115 ], IL18R1 [ 116 ], KCNA7 [ 117 ] and CALCRL (calcitonin receptor like receptor) [ 118 ] have an important role in HF. Li et al [ 119 ], Deckx et al [ 120 ], Ichihara et al [ 121 ] and Paik et al [ 122 ] showed that the SERPINE2, OGN (osteoglycin), AGTR2 and WNT10B promoted cardiac interstitial fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Identification of candidate biomarkers and therapeutic agents for heart failure by bioinformatics analysis

Kolur¹,

Vastrad²,

Vastrad

et al. 2021

BMC Cardiovasc Disord

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Introduction Heart failure (HF) is a heterogeneous clinical syndrome and affects millions of people all over the world. HF occurs when the cardiac overload and injury, which is a worldwide complaint. The aim of this study was to screen and verify hub genes involved in developmental HF as well as to explore active drug molecules. Methods The expression profiling by high throughput sequencing of GSE141910 dataset was downloaded from the Gene Expression Omnibus (GEO) database, which contained 366 samples, including 200 heart failure samples and 166 non heart failure samples. The raw data was integrated to find differentially expressed genes (DEGs) and were further analyzed with bioinformatics analysis. Gene ontology (GO) and REACTOME enrichment analyses were performed via ToppGene; protein–protein interaction (PPI) networks of the DEGs was constructed based on data from the HiPPIE interactome database; modules analysis was performed; target gene—miRNA regulatory network and target gene—TF regulatory network were constructed and analyzed; hub genes were validated; molecular docking studies was performed. Results A total of 881 DEGs, including 442 up regulated genes and 439 down regulated genes were observed. Most of the DEGs were significantly enriched in biological adhesion, extracellular matrix, signaling receptor binding, secretion, intrinsic component of plasma membrane, signaling receptor activity, extracellular matrix organization and neutrophil degranulation. The top hub genes ESR1, PYHIN1, PPP2R2B, LCK, TP63, PCLAF, CFTR, TK1, ECT2 and FKBP5 were identified from the PPI network. Module analysis revealed that HF was associated with adaptive immune system and neutrophil degranulation. The target genes, miRNAs and TFs were identified from the target gene—miRNA regulatory network and target gene—TF regulatory network. Furthermore, receiver operating characteristic (ROC) curve analysis and RT-PCR analysis revealed that ESR1, PYHIN1, PPP2R2B, LCK, TP63, PCLAF, CFTR, TK1, ECT2 and FKBP5 might serve as prognostic, diagnostic biomarkers and therapeutic target for HF. The predicted targets of these active molecules were then confirmed. Conclusion The current investigation identified a series of key genes and pathways that might be involved in the progression of HF, providing a new understanding of the underlying molecular mechanisms of HF.

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“…Increased LA was also associated with the occurrence of AF and acute heart failure ( Oikonomou et al, 2019 ; Van Aelst et al, 2018 ), while low ALB level was an important predictor for poor prognosis after cardiac surgery ( Van Beek et al, 2018 ). ApoA1 was an apolipoprotein of HDL which has anti-inflammatory and antioxidant effects ( Gombos et al, 2017 ). TREM1 was related to these markers associated with adverse outcome of cardiac diseases, so we hypothesized that TREM1 may also be associated with the prognosis of myocardial infarction, which was also confirmed by the follow-up results.…”

Section: Discussionmentioning

confidence: 99%

Accuracy of triggering receptor expressed on myeloid cells 1 in diagnosis and prognosis of acute myocardial infarction: a prospective cohort study

Ji¹,

Zhang²,

Yang³

et al. 2021

PeerJ

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Background Acute myocardial infarction (AMI) is one of the fatal cardiac emergencies. The detection of triggering receptor expressed on myeloid cells 1 (TREM1), a cell surface immunoglobulin that amplifies pro-inflammatory responses, screened by bioinformatics was shown to be significant in diagnosing and predicting the prognosis of AMI. Methods GSE66360, GSE61144 and GSE60993 were downloaded from the Gene Expression Omnibus (GEO) database to explore the differentially expressed genes (DEGs) between AMI and control groups using R software. A total of 147 patients in total were prospectively enrolled from October 2018 to June 2019 and divided into two groups, the normal group (n = 35) and the AMI group (n = 112). Plasma was collected from each patient at admission and all patients received 6-month follow-up care. Results According to bioinformatic analysis, TREM1 was an important DEG in patients with AMI. Compared with the normal group, TREM1 expression was markedly increased in the AMI group (p < 0.001). TREM1 expression was positively correlated with fasting plasma glucose (FPG), glycosylated hemoglobin (HbAC), and the number of lesion vessels, although it had no correlation with Gensini score. TREM1 expression in the triple-vessels group was significantly higher than that of the single-vessel group (p < 0.05). Multiple linear regression showed that UA and HbAC were two factors influencing TREM1 expression. The ROC curve showed that TREM1 had a diagnostic significance in AMI (p < 0.001), especially in AMI patients without diabetes. Cox regression showed increased TREM1 expression was closely associated with 6-month major adverse cardiac events (MACEs) (p < 0.001). Conclusions TREM1 is a potentially significant biomarker for the diagnosis of AMI and may be closely associated with the severity of coronary lesions and diabetes. TREM1 may also be helpful in predicting the 6-month MACEs after AMI.

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Long-Term Survival and Apolipoprotein A1 Level in Chronic Heart Failure: Interaction With Tumor Necrosis Factor α −308 G/A Polymorphism

Cited by 20 publications

References 25 publications

Low-density lipoprotein cholesterol and survival in pulmonary arterial hypertension

Low-density lipoprotein cholesterol and survival in pulmonary arterial hypertension

Identification of candidate biomarkers and therapeutic agents for heart failure by bioinformatics analysis

Accuracy of triggering receptor expressed on myeloid cells 1 in diagnosis and prognosis of acute myocardial infarction: a prospective cohort study

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