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Article ; Online: Biomarker and transcriptomics profiles of serum selenium concentrations in patients with heart failure are associated with immunoregulatory processes.

Al-Mubarak, Ali A / Markousis Mavrogenis, George / Guo, Xuanxuan / De Bruyn, Marco / Nath, Mintu / Romaine, Simon P R / Grote Beverborg, Niels / Arevalo Gomez, Karla / Zijlstra, Sietske N / van Veldhuisen, Dirk J / Samani, Nilesh J / Voors, Adriaan A / van der Meer, Peter / Bomer, Nils

Redox biology

2024 Volume 70, Page(s) 103046

Abstract: ... selenium status (P: Conclusion: These data suggest that immunoregulation is an important mechanism ...

Abstract	Background: Low selenium concentrations are associated with worse outcomes in heart failure (HF). However, the underlying pathophysiologic mechanisms remain incompletely understood. Therefore, we aimed to contrast serum selenium concentrations to blood biomarker and transcriptomic profiles in patients with HF. Methods: Circulating biomarkers, whole blood transcriptomics and serum selenium measurements in a cohort of 2328 patients with HF were utilized. Penalized linear regression and gene expression analysis were used to assess biomarker and transcriptomics profiles, respectively. As a proof-of-principle, potential causal effects of selenium on excreted cytokines concentrations were investigated using human peripheral blood mononuclear cells (PBMCs). Results: Mean selenium levels were 60.6 μg/L in Q1 and 122.0 μg/L in Q4. From 356 biomarkers and 20 clinical features, the penalized linear regression model yielded 44 variables with <5 % marginal false discovery rate as predictors of serum selenium. Biomarkers associated positively with selenium concentrations included: epidermal growth factor receptor (EGFR), IFN-gamma-R1, CD4, GDF15, and IL10. Biomarkers associated negatively with selenium concentrations included: PCSK9, TNFSF13, FGF21 and PAI. Additionally, 148 RNA transcripts were found differentially expressed between high and low selenium status (P Conclusion: These data suggest that immunoregulation is an important mechanism through which selenium might have beneficial roles in HF. The beneficial effects of higher serum selenium concentrations are likely because of global immunomodulatory effects on the abundance of cytokines. MSRB1 and GPX4 are potential modulators of and should be pursued in future research.
MeSH term(s)	Humans ; Selenium/metabolism ; Proprotein Convertase 9/metabolism ; Transcriptome ; Leukocytes, Mononuclear/metabolism ; Biomarkers ; Gene Expression Profiling ; Heart Failure/genetics ; Cytokines ; RNA
Chemical Substances	Selenium (H6241UJ22B) ; PCSK9 protein, human (EC 3.4.21.-) ; Proprotein Convertase 9 (EC 3.4.21.-) ; Biomarkers ; Cytokines ; RNA (63231-63-0)
Language	English
Publishing date	2024-01-26
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2024.103046
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Article ; Online: A multi-omics glimpse into the biology of arterial stiffness.

Eales, James M / Romaine, Simon P R / Charchar, Fadi J / Tomaszewski, Maciej

Journal of hypertension

2015 Volume 34, Issue 1, Page(s) 32–35

Language	English
Publishing date	2015-11-27
Publishing country	England
Document type	Comment ; Editorial
ZDB-ID	605532-1
ISSN	1473-5598 ; 0263-6352 ; 0952-1178
ISSN (online)	1473-5598
ISSN	0263-6352 ; 0952-1178
DOI	10.1097/HJH.0000000000000783
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Article ; Online: Circulating microRNAs and hypertension--from new insights into blood pressure regulation to biomarkers of cardiovascular risk.

Romaine, Simon P R / Charchar, Fadi J / Samani, Nilesh J / Tomaszewski, Maciej

Current opinion in pharmacology

2016 Volume 27, Page(s) 1–7

Abstract: Hypertension is a leading cause of cardiovascular morbidity and mortality worldwide, yet the molecular mechanisms underpinning the development of high blood pressure remain incompletely understood. MicroRNAs are small, non-coding RNA molecules ... ...

Abstract	Hypertension is a leading cause of cardiovascular morbidity and mortality worldwide, yet the molecular mechanisms underpinning the development of high blood pressure remain incompletely understood. MicroRNAs are small, non-coding RNA molecules approximately 22 nucleotides in length that act as post-transcriptional regulators of gene expression. We highlight, through a review of recent literature, that studies on circulating microRNAs have provided novel insights into blood pressure regulation. They have also complemented tissue-based and animal-based experiments in shedding new light on our understanding of established pathways in hypertension, such as the renin-angiotensin system. Despite a number of challenges, we believe microRNAs herald particular potential in becoming effective biomarkers of target-organ damage in hypertension.
MeSH term(s)	Animals ; Biomarkers/blood ; Blood Pressure/physiology ; Cardiovascular Diseases/blood ; Cardiovascular Diseases/etiology ; Cardiovascular System/physiopathology ; Humans ; Hypertension/blood ; Hypertension/physiopathology ; MicroRNAs/blood ; Risk Factors
Chemical Substances	Biomarkers ; MicroRNAs
Language	English
Publishing date	2016-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2037057-X
ISSN	1471-4973 ; 1471-4892
ISSN (online)	1471-4973
ISSN	1471-4892
DOI	10.1016/j.coph.2015.12.002
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Article ; Online: MicroRNAs in cardiovascular disease: an introduction for clinicians.

Romaine, Simon P R / Tomaszewski, Maciej / Condorelli, Gianluigi / Samani, Nilesh J

Heart (British Cardiac Society)

2015 Volume 101, Issue 12, Page(s) 921–928

Abstract: MicroRNAs (miRNAs) are small, non-coding, RNA molecules approximately 22 nucleotides in length which act as post-transcriptional regulators of gene expression. Individual miRNAs have been shown to regulate the expression of multiple genes. Conversely, ... ...

Abstract	MicroRNAs (miRNAs) are small, non-coding, RNA molecules approximately 22 nucleotides in length which act as post-transcriptional regulators of gene expression. Individual miRNAs have been shown to regulate the expression of multiple genes. Conversely, the expression of individual genes can be regulated by multiple miRNAs. Consequently, since their discovery just over 20 years ago, miRNAs have been identified as key regulators of complex biological processes linked to multiple cardiovascular pathologies, including left ventricular hypertrophy, ischaemic heart disease, heart failure, hypertension and arrhythmias. Furthermore, since the finding that miRNAs are present in the circulation, they have been investigated as novel biomarkers, especially in the context of acute myocardial infarction (AMI) and heart failure. While there is little convincing evidence that miRNAs can outperform traditional biomarkers, such as cardiac troponins, in the diagnosis of AMI, there is potential for miRNAs to complement existing risk prediction models and act as valuable markers of post-AMI prognosis. Encouragingly, the concept of miRNA-based therapeutics is developing, with synthetic antagonists of miRNAs (antagomiRs) currently in phase II trials for the treatment of chronic hepatitis C virus infection. In the cardiovascular field, promising preclinical studies suggest that they could be useful in treating disorders ranging from heart failure to dyslipidaemia, although several challenges related to specificity and targeted delivery remain to be overcome. Through this review, we provide clinicians with a brief overview of the ever-expanding world of miRNAs.
MeSH term(s)	Adult ; Animals ; Atherosclerosis/physiopathology ; Atrial Remodeling/physiology ; Cardiovascular Diseases/drug therapy ; Cardiovascular Diseases/genetics ; Cardiovascular Diseases/metabolism ; Humans ; MicroRNAs/analysis ; MicroRNAs/genetics ; MicroRNAs/physiology ; Molecular Targeted Therapy
Chemical Substances	MicroRNAs
Language	English
Publishing date	2015-03-26
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1303417-0
ISSN	1468-201X ; 1355-6037
ISSN (online)	1468-201X
ISSN	1355-6037
DOI	10.1136/heartjnl-2013-305402
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Article ; Online: Whole blood transcriptomic profiling identifies molecular pathways related to cardiovascular mortality in heart failure.

European journal of heart failure

2022 Volume 24, Issue 6, Page(s) 1009–1019

Abstract: Aims: Chronic heart failure (CHF) is a systemic syndrome with a poor prognosis and a need for novel therapies. We investigated whether whole blood transcriptomic profiling can provide new mechanistic insights into cardiovascular (CV) mortality in CHF.!## ...

Abstract	Aims: Chronic heart failure (CHF) is a systemic syndrome with a poor prognosis and a need for novel therapies. We investigated whether whole blood transcriptomic profiling can provide new mechanistic insights into cardiovascular (CV) mortality in CHF. Methods and results: Transcriptome profiles were generated at baseline from 944 CHF patients from the BIOSTAT-CHF study, of whom 626 survived and 318 died from a CV cause during a follow-up of 21 months. Multivariable analysis, including adjustment for cell count, identified 1153 genes (6.5%) that were differentially expressed between those that survived or died and strongly related to a validated clinical risk score for adverse prognosis. The differentially expressed genes mainly belonged to five non-redundant pathways: adaptive immune response, proteasome-mediated ubiquitin-dependent protein catabolic process, T-cell co-stimulation, positive regulation of T-cell proliferation, and erythrocyte development. These five pathways were selectively related (RV coefficients >0.20) with seven circulating protein biomarkers of CV mortality (fibroblast growth factor 23, soluble ST2, adrenomedullin, hepcidin, pentraxin-3, WAP 4-disulfide core domain 2, and interleukin-6) revealing an intricate relationship between immune and iron homeostasis. The pattern of survival-associated gene expression matched with 29 perturbagen-induced transcriptome signatures in the iLINCS drug-repurposing database, identifying drugs, approved for other clinical indications, that were able to reverse in vitro the molecular changes associated with adverse prognosis in CHF. Conclusion: Systematic modelling of the whole blood protein-coding transcriptome defined molecular pathways that provide a link between clinical risk factors and adverse CV prognosis in CHF, identifying both established and new potential therapeutic targets.
MeSH term(s)	Biomarkers ; Chronic Disease ; Heart Failure ; Humans ; Prognosis ; Transcriptome
Chemical Substances	Biomarkers
Language	English
Publishing date	2022-06-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1483672-5
ISSN	1879-0844 ; 1388-9842
ISSN (online)	1879-0844
ISSN	1388-9842
DOI	10.1002/ejhf.2540
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Article ; Online: Clinical implications of low estimated protein intake in patients with heart failure.

Streng, Koen W / Hillege, Hans L / Ter Maaten, Jozine M / van Veldhuisen, Dirk J / Dickstein, Kenneth / Ng, Leong L / Samani, Nilesh J / Metra, Marco / Ponikowski, Piotr / Cleland, John G / Anker, Stefan D / Romaine, Simon P R / Damman, Kevin / van der Meer, Peter / Lang, Chim C / Voors, Adriaan A

Journal of cachexia, sarcopenia and muscle

2022 Volume 13, Issue 3, Page(s) 1762–1770

Abstract: ... with 18% in the highest quartile (P < 0.001). In a multivariable model, lower estimated protein intake was ... confidence interval (CI) 1.03-2.18, P = 0.036 for the lowest quartile and HR 1.46; 95% CI 1.00-2.18, P = 0.049 ...

Abstract	Background: A higher protein intake has been associated with a higher muscle mass and lower mortality rates in the general population, but data about protein intake and survival in patients with heart failure (HF) are lacking. Methods: We studied the prevalence, predictors, and clinical outcome of estimated protein intake in 2516 patients from the BIOlogy Study to TAilored Treatment in Chronic Heart Failure (BIOSTAT-CHF) index cohort. Protein intake was calculated in spot urine samples using a validated formula [13.9 + 0.907 * body mass index (BMI) (kg/m Results: We included 2282 HF patients (mean age 68 ± 12 years and 27% female). Lower estimated protein intake in HF patients was associated with a lower BMI, but with more signs of congestion. Mortality rate in the lowest quartile was 32%, compared with 18% in the highest quartile (P < 0.001). In a multivariable model, lower estimated protein intake was associated with a higher risk of death compared with the highest quartile [hazard ratio (HR) 1.50; 95% confidence interval (CI) 1.03-2.18, P = 0.036 for the lowest quartile and HR 1.46; 95% CI 1.00-2.18, P = 0.049 for the second quartile]. Conclusions: An estimated lower protein intake was associated with a lower BMI, but signs of congestion were more prevalent. A lower estimated protein intake was independently associated with a higher mortality risk.
MeSH term(s)	Aged ; Aged, 80 and over ; Body Mass Index ; Cohort Studies ; Female ; Heart Failure/metabolism ; Humans ; Male ; Middle Aged ; Proportional Hazards Models ; Prospective Studies
Language	English
Publishing date	2022-04-14
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2586864-0
ISSN	2190-6009 ; 2190-5991
ISSN (online)	2190-6009
ISSN	2190-5991
DOI	10.1002/jcsm.12973
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Article ; Online: Multiomics Analysis Provides Novel Pathways Related to Progression of Heart Failure.

Ouwerkerk, Wouter / Belo Pereira, Joao P / Maasland, Troy / Emmens, Johanna E / Figarska, Sylwia M / Tromp, Jasper / Koekemoer, Andrea L / Nelson, Christopher P / Nath, Mintu / Romaine, Simon P R / Cleland, John G F / Zannad, Faiez / van Veldhuisen, Dirk J / Lang, Chim C / Ponikowski, Piotr / Filippatos, Gerasimos / Anker, Stefan / Metra, Marco / Dickstein, Kenneth /

Ng, Leong L / de Boer, Rudolf A / van Riel, Natal / Nieuwdorp, Max / Groen, Albert K / Stroes, Erik / Zwinderman, Aeilko H / Samani, Nilesh J / Lam, Carolyn S P / Levin, Evgeni / Voors, Adriaan A

Journal of the American College of Cardiology

2023 Volume 82, Issue 20, Page(s) 1921–1931

Abstract: Background: Despite major advances in pharmacological treatment for patients with heart failure, residual mortality remains high. This suggests that important pathways are not yet targeted by current heart failure therapies.: Objectives: We sought ... ...

Abstract	Background: Despite major advances in pharmacological treatment for patients with heart failure, residual mortality remains high. This suggests that important pathways are not yet targeted by current heart failure therapies. Objectives: We sought integration of genetic, transcriptomic, and proteomic data in a large cohort of patients with heart failure to detect major pathways related to progression of heart failure leading to death. Methods: We used machine learning methodology based on stacked generalization framework and gradient boosting algorithms, using 54 clinical phenotypes, 403 circulating plasma proteins, 36,046 transcript expression levels in whole blood, and 6 million genomic markers to model all-cause mortality in 2,516 patients with heart failure from the BIOSTAT-CHF (Systems BIOlogy Study to TAilored Treatment in Chronic Heart Failure) study. Results were validated in an independent cohort of 1,738 patients. Results: The mean age of the patients was 70 years (Q1-Q3: 61-78 years), 27% were female, median N-terminal pro-B-type natriuretic peptide was 4,275 ng/L (Q1-Q3: 2,360-8,486 ng/L), and 7% had heart failure with preserved ejection fraction. During a median follow-up of 21 months, 657 (26%) of patients died. The 4 major pathways with a significant association to all-cause mortality were: 1) the PI3K/Akt pathway; 2) the MAPK pathway; 3) the Ras signaling pathway; and 4) epidermal growth factor receptor tyrosine kinase inhibitor resistance. Results were validated in an independent cohort of 1,738 patients. Conclusions: A systems biology approach integrating genomic, transcriptomic, and proteomic data identified 4 major pathways related to mortality. These pathways are related to decreased activation of the cardioprotective ERBB2 receptor, which can be modified by neuregulin.
MeSH term(s)	Humans ; Female ; Aged ; Male ; Biomarkers ; Proteomics ; Multiomics ; Phosphatidylinositol 3-Kinases/therapeutic use ; Heart Failure/drug therapy
Chemical Substances	Biomarkers ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-)
Language	English
Publishing date	2023-11-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	605507-2
ISSN	1558-3597 ; 0735-1097
ISSN (online)	1558-3597
ISSN	0735-1097
DOI	10.1016/j.jacc.2023.08.053
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Article ; Online: Telomere length is independently associated with all-cause mortality in chronic heart failure.

Heart (British Cardiac Society)

2021 Volume 108, Issue 2, Page(s) 124–129

Abstract: ... 1.16 (95% CI 1.08 to 1.24); p=2.66×10: Conclusion: In patients with heart failure, shorter mean ...

Abstract	Objective: Patients with heart failure have shorter mean leucocyte telomere length (LTL), a marker of biological age, compared with healthy subjects, but it is unclear whether this is of prognostic significance. We therefore sought to determine whether LTL is associated with outcomes in patients with heart failure. Methods: We measured LTL in patients with heart failure from the BIOSTAT-CHF Index (n=2260) and BIOSTAT-CHF Tayside (n=1413) cohorts. Cox proportional hazards analyses were performed individually in each cohort and the estimates combined using meta-analysis. Our co-primary endpoints were all-cause mortality and heart failure hospitalisation. Results: In age-adjusted and sex-adjusted analyses, shorter LTL was associated with higher all-cause mortality in both cohorts individually and when combined (meta-analysis HR (per SD decrease in LTL)=1.16 (95% CI 1.08 to 1.24); p=2.66×10 Conclusion: In patients with heart failure, shorter mean LTL is independently associated with all-cause mortality.
MeSH term(s)	Chronic Disease ; Cohort Studies ; Heart Failure/diagnosis ; Heart Failure/genetics ; Humans ; Leukocytes ; Risk Factors ; Telomere/genetics
Language	English
Publishing date	2021-03-31
Publishing country	England
Document type	Journal Article ; Meta-Analysis ; Research Support, Non-U.S. Gov't
ZDB-ID	1303417-0
ISSN	1468-201X ; 1355-6037
ISSN (online)	1468-201X
ISSN	1355-6037
DOI	10.1136/heartjnl-2020-318654
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Article ; Online: Bio-adrenomedullin as a marker of congestion in patients with new-onset and worsening heart failure.

Ter Maaten, Jozine M / Kremer, Daan / Demissei, Biniyam G / Struck, Joachim / Bergmann, Andreas / Anker, Stefan D / Ng, Leong L / Dickstein, Kenneth / Metra, Marco / Samani, Nilesh J / Romaine, Simon P R / Cleland, John / Girerd, Nicolas / Lang, Chim C / van Veldhuisen, Dirk J / Voors, Adriaan A

European journal of heart failure

2019 Volume 21, Issue 6, Page(s) 732–743

Abstract: ... more signs and symptoms of congestion (all P < 0.001). Amongst 20 biomarkers, bio-ADM was the strongest ... predictor of a clinical congestion score (r: Conclusions: Plasma bio-ADM in patients with new-onset and ...

Abstract	Background: Secretion of adrenomedullin (ADM) is stimulated by volume overload to maintain endothelial barrier function, and higher levels of biologically active (bio-) ADM in heart failure (HF) are a counteracting response to vascular leakage and tissue oedema. This study aimed to establish the value of plasma bio-ADM as a marker of congestion in patients with worsening HF. Methods and results: The association of plasma bio-ADM with clinical markers of congestion, as well as its prognostic value was studied in 2179 patients with new-onset or worsening HF enrolled in BIOSTAT-CHF. Data were validated in a separate cohort of 1703 patients. Patients with higher plasma bio-ADM levels were older, had more severe HF and more signs and symptoms of congestion (all P < 0.001). Amongst 20 biomarkers, bio-ADM was the strongest predictor of a clinical congestion score (r Conclusions: Plasma bio-ADM in patients with new-onset and worsening HF is associated with more severe HF and more oedema, orthopnoea, hepatomegaly and jugular venous pressure. We therefore postulate bio-ADM as a congestion marker, which might become useful to guide decongestive therapy.
MeSH term(s)	Adrenomedullin/blood ; Aged ; Aged, 80 and over ; Biomarkers/blood ; Cohort Studies ; Disease Progression ; Female ; Heart Failure/blood ; Heart Failure/complications ; Heart Failure/physiopathology ; Humans ; Male ; Middle Aged ; Predictive Value of Tests ; Prognosis ; Stroke Volume/physiology
Chemical Substances	Biomarkers ; Adrenomedullin (148498-78-6)
Language	English
Publishing date	2019-03-06
Publishing country	England
Document type	Journal Article ; Multicenter Study ; Observational Study ; Research Support, Non-U.S. Gov't
ZDB-ID	1483672-5
ISSN	1879-0844 ; 1388-9842
ISSN (online)	1879-0844
ISSN	1388-9842
DOI	10.1002/ejhf.1437
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Article ; Online: A network analysis to identify pathophysiological pathways distinguishing ischaemic from non-ischaemic heart failure.

Sama, Iziah E / Woolley, Rebecca J / Nauta, Jan F / Romaine, Simon P R / Tromp, Jasper / Ter Maaten, Jozine M / van der Meer, Peter / Lam, Carolyn S P / Samani, Nilesh J / Ng, Leong L / Metra, Marco / Dickstein, Kenneth / Anker, Stefan D / Zannad, Faiez / Lang, Chim C / Cleland, John G F / van Veldhuisen, Dirk J / Hillege, Hans L / Voors, Adriaan A

European journal of heart failure

2020 Volume 22, Issue 5, Page(s) 821–833

Abstract: Aims: Heart failure (HF) is frequently caused by an ischaemic event (e.g. myocardial infarction) but might also be caused by a primary disease of the myocardium (cardiomyopathy). In order to identify targeted therapies specific for either ischaemic or ... ...

Abstract	Aims: Heart failure (HF) is frequently caused by an ischaemic event (e.g. myocardial infarction) but might also be caused by a primary disease of the myocardium (cardiomyopathy). In order to identify targeted therapies specific for either ischaemic or non-ischaemic HF, it is important to better understand differences in underlying molecular mechanisms. Methods and results: We performed a biological physical protein-protein interaction network analysis to identify pathophysiological pathways distinguishing ischaemic from non-ischaemic HF. First, differentially expressed plasma protein biomarkers were identified in 1160 patients enrolled in the BIOSTAT-CHF study, 715 of whom had ischaemic HF and 445 had non-ischaemic HF. Second, we constructed an enriched physical protein-protein interaction network, followed by a pathway over-representation analysis. Finally, we identified key network proteins. Data were validated in an independent HF cohort comprised of 765 ischaemic and 100 non-ischaemic HF patients. We found 21/92 proteins to be up-regulated and 2/92 down-regulated in ischaemic relative to non-ischaemic HF patients. An enriched network of 18 proteins that were specific for ischaemic heart disease yielded six pathways, which are related to inflammation, endothelial dysfunction superoxide production, coagulation, and atherosclerosis. We identified five key network proteins: acid phosphatase 5, epidermal growth factor receptor, insulin-like growth factor binding protein-1, plasminogen activator urokinase receptor, and secreted phosphoprotein 1. Similar results were observed in the independent validation cohort. Conclusions: Pathophysiological pathways distinguishing patients with ischaemic HF from those with non-ischaemic HF were related to inflammation, endothelial dysfunction superoxide production, coagulation, and atherosclerosis. The five key pathway proteins identified are potential treatment targets specifically for patients with ischaemic HF.
MeSH term(s)	Aged ; Angiotensin Receptor Antagonists ; Angiotensin-Converting Enzyme Inhibitors ; Female ; Heart Failure/diagnosis ; Humans ; Male ; Middle Aged ; Percutaneous Coronary Intervention ; Stroke Volume ; Ventricular Function, Left
Chemical Substances	Angiotensin Receptor Antagonists ; Angiotensin-Converting Enzyme Inhibitors
Language	English
Publishing date	2020-04-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1483672-5
ISSN	1879-0844 ; 1388-9842
ISSN (online)	1879-0844
ISSN	1388-9842
DOI	10.1002/ejhf.1811
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