Special Issue "Biomolecules for Translational Approaches in Cardiology"

A special issue of Biomolecules (ISSN 2218-273X).

Deadline for manuscript submissions: 30 November 2018

Special Issue Editors

Guest Editor
Dr. Mahir Karakas

Clinic for General and Interventional Cardiology, University Heart Center Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg, Germany
Website | E-Mail
Interests: biomarkers in cardiology; clinical trials in cardiology; genomics in cardiology; genetic epidemiology; cardiology
Guest Editor
Prof. Dr. Tanja Zeller

Clinic for General and Interventional Cardiology, University Heart Center Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg, Germany
Website | E-Mail
Interests: systems medince; genomics and genetics in cardiology; biomarkers in cardiology; genetic epidemiology

Special Issue Information

Dear Colleagues, 

Over the last few years, biomarker research has improved our knowledge about the pathomechanisms and risk assessment in the cardiovascular field. Increasing our understanding of the multifactorial, complex underpinnings of cardiovascular diseases promises to have a global impact on the promotion of health. Valuable insights have already been acquired from several genomic and genetic studies and novel molecular biomarkers have been associated with cardiovascular risk. Translational approaches into a full understanding of the underlying mechanisms of biomarkers and into their clinical relevance are currently ongoing. The systematic integration of multidimensional biomarker datasets, such as genomics, transcriptomics and proteomics evolves as the next challenge, including molecular findings of interactions between biomolecules as well as knowledge from cell biology, animal experiments and human phenotypic and clinical data. We encourage scientists of diverse backgrounds (clinics, systems medicine, genetics, molecular biology, epidemiology) and working in the cardiovascular field to contribute original research or review articles covering studies on biomolecule identification or characterization and translational approaches of clinical relevance. 

Dr. Mahir Karakas
Prof. Dr. Tanja Zeller
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 650 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cardiovascular biomarkers
  • systems medicine
  • genomics and genetics
  • epidemiology
  • cardiology
  • clinical trials
  • clinical translation

Published Papers (13 papers)

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Research

Jump to: Review

Open AccessArticle Add-on Immunoadsorption Shortly-after Optimal Medical Treatment Further Significantly and Persistently Improves Cardiac Function and Symptoms in Recent-Onset Heart Failure—A Single Center Experience
Biomolecules 2018, 8(4), 133; https://doi.org/10.3390/biom8040133
Received: 4 September 2018 / Revised: 17 October 2018 / Accepted: 29 October 2018 / Published: 2 November 2018
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Abstract
Background: Immunoadsorption and intravenous immunoglobulin (IVIG) administration may have beneficial effects in patients with dilated cardiomyopathy with end-stage heart failure. We investigated the effect of immunoadsorption with subsequent IVIG administration on cardiac function and symptoms in patients on optimal medical treatment (OMT) for
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Background: Immunoadsorption and intravenous immunoglobulin (IVIG) administration may have beneficial effects in patients with dilated cardiomyopathy with end-stage heart failure. We investigated the effect of immunoadsorption with subsequent IVIG administration on cardiac function and symptoms in patients on optimal medical treatment (OMT) for heart failure (HF) with recent-onset cardiomyopathy during long-term follow-up. Methods: Thirty-five patients with recent-onset of HF symptoms received intensive guideline-recommended medical HF therapy for 5.2 months. Subsequently, all patients received a single cycle of immunoadsorption for five days followed by IVIG administration. During the 29-month follow-up period, New York Heart Association (NYHA) functional class, left ventricular ejection fraction (LVEF) and N-terminal pro brain natriuretic peptide (NT-proBNP) were evaluated. Changes in quality of life (QoL) were assessed using the Minnesota Living with HF Questionnaire. Results: Three months after immunoadsorption, NYHA functional class improved from 2.0 to 1.5 (p < 0.005) and LVEF significantly increased from 27.0% to 39.0% (p < 0.0001). Long-term follow-up of 29 months showed stable NYHA functional class and a further moderate increase in LVEF from 39.0% to 42.0% (p < 0.0001) accompanied by a significant improvement in NT-proBNP and QoL scores. Conclusion: Immunoadsorption followed by IVIG administration further enhances LVEF, HF symptoms, QoL and biomarkers in patients with recent-onset HF on OMT. Full article
(This article belongs to the Special Issue Biomolecules for Translational Approaches in Cardiology)
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Open AccessArticle Cross-Sectional Associations between Homoarginine, Intermediate Phenotypes, and Atrial Fibrillation in the Community—The Gutenberg Health Study
Biomolecules 2018, 8(3), 86; https://doi.org/10.3390/biom8030086
Received: 11 July 2018 / Revised: 26 August 2018 / Accepted: 27 August 2018 / Published: 30 August 2018
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Abstract
Homoarginine has come into the focus of interest as a biomarker for cardiovascular disease. Atrial fibrillation (AF) causes a substantial increase in morbidity and mortality. Whether circulating homoarginine is associated with occurrence or persistence of AF and may serve as a new predictive
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Homoarginine has come into the focus of interest as a biomarker for cardiovascular disease. Atrial fibrillation (AF) causes a substantial increase in morbidity and mortality. Whether circulating homoarginine is associated with occurrence or persistence of AF and may serve as a new predictive biomarker remains unknown. We measured plasma levels of homoarginine in the population-based Gutenberg health study (3761 patients included, of them 51.7% males), mean age 55.6 ± 10.9 years-old. Associations between homoarginine and intermediate electrocardiographic and echocardiographic phenotypes and manifest AF were examined. Patients with AF (124 patients, of them 73.4% males) had a mean age 64.8 ± 8.6 years-old compared to a mean age of 55.3 ± 10.9 in the population without AF (p-value < 0.001) and showed a less beneficial risk factor profile. The median homoarginine levels in individuals with and without AF were 1.9 μmol/L (interquartile range (IQR) 1.5–2.5) and 2.0 μmol/L (IQR 1.5–2.5), respectively, p = 0.56. In multivariable-adjusted regression analyses homoarginine was not statistically significantly related to electrocardiographic variables. Among echocardiographic variables beta per standard deviation increase was −0.12 (95% confidence interval (CI) −0.23–(−0.02); p = 0.024) for left atrial area and −0.01 (95% CI −0.02–(−0.003); p = 0.013) for E/A ratio. The odds ratio between homoarginine and AF was 0.91 (95% CI 0.70–1.16; p = 0.45). In our large, population-based cross-sectional study, we did not find statistically significant correlations between lower homoarginine levels and occurrence or persistence of AF or most standard electrocardiographic phenotypes, but some moderate inverse associations with echocardiographic left atrial size and E/A. Homoarginine may not represent a strong biomarker to identify individuals at increased risk for AF. Further investigations will be needed to elucidate the role of homoarginine and cardiac function. Full article
(This article belongs to the Special Issue Biomolecules for Translational Approaches in Cardiology)
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Open AccessArticle Testosterone Levels and Type 2 Diabetes—No Correlation with Age, Differential Predictive Value in Men and Women
Biomolecules 2018, 8(3), 76; https://doi.org/10.3390/biom8030076
Received: 8 June 2018 / Revised: 3 August 2018 / Accepted: 13 August 2018 / Published: 20 August 2018
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Abstract
Most studies reporting on the association of circulating testosterone levels with type 2 diabetes in men are of cross-sectional design. Reports on the relevance of altered testosterone levels in women are scarce. Here, we evaluate the role of low serum testosterone levels for
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Most studies reporting on the association of circulating testosterone levels with type 2 diabetes in men are of cross-sectional design. Reports on the relevance of altered testosterone levels in women are scarce. Here, we evaluate the role of low serum testosterone levels for incident diabetes in men and women in a population setting of 7706 subjects (3896 females). During a mean follow up time of 13.8 years, 7.8% developed type 2 diabetes. Significant correlations of testosterone with high density lipoprotein (HDL)-cholesterol (R = 0.21, p < 0.001), body-mass-index (R = −0.23, p < 0.001), and waist-to-hip-ratio (R = −0.21, p < 0.001) were found in men. No correlation was found with age in men; in women, the correlation was negligible (R = 0.04, p = 0.012). In men, low testosterone levels predicted high risk of type 2 diabetes, while in women this relationship was opposite. Men with low testosterone levels showed increased risk of future diabetes (hazard ratio (HR) 2.66, 95% confidence interval (CI) 1.91–3.72, p < 0.001 in basic model; HR 1.56 95%, CI 1.10–2.21, p = 0.003). In women, low testosterone levels indicated lower risk with (HR 0.53, 95% CI 0.37–0.77, p = 0.003), while the association lost significance in the fully adjusted model (HR 0.72, 95% CI 0.49–1.05, p = 0.09). Low levels of testosterone predicted future diabetes in men. A borderline opposite association was found in women. Full article
(This article belongs to the Special Issue Biomolecules for Translational Approaches in Cardiology)
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Open AccessArticle Novel DNA Methylation Sites Influence GPR15 Expression in Relation to Smoking
Biomolecules 2018, 8(3), 74; https://doi.org/10.3390/biom8030074
Received: 16 July 2018 / Revised: 6 August 2018 / Accepted: 9 August 2018 / Published: 20 August 2018
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Abstract
Smoking is a major risk factor for cardiovascular diseases and has been implicated in the regulation of the G protein-coupled receptor 15 (GPR15) by affecting CpG methylation. The G protein-coupled receptor 15 is involved in angiogenesis and inflammation. An effect on GPR15 gene
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Smoking is a major risk factor for cardiovascular diseases and has been implicated in the regulation of the G protein-coupled receptor 15 (GPR15) by affecting CpG methylation. The G protein-coupled receptor 15 is involved in angiogenesis and inflammation. An effect on GPR15 gene regulation has been shown for the CpG site CpG3.98251294. We aimed to analyze the effect of smoking on GPR15 expression and methylation sites spanning the GPR15 locus. DNA methylation of nine GPR15 CpG sites was measured in leukocytes from 1291 population-based individuals using the EpiTYPER. Monocytic GPR15 expression was measured by qPCR at baseline and five-years follow up. GPR15 gene expression was upregulated in smokers (beta (ß) = −2.699, p-value (p) = 1.02 × 10−77) and strongly correlated with smoking exposure (ß = −0.063, p = 2.95 × 10−34). Smoking cessation within five years reduced GPR15 expression about 19% (p = 9.65 × 10−5) with decreasing GPR15 expression over time (ß = 0.031, p = 3.81 × 10−6). Additionally, three novel CpG sites within GPR15 affected by smoking were identified. For CpG3.98251047, DNA methylation increased steadily after smoking cessation (ß = 0.123, p = 1.67 × 10−3) and strongly correlated with changes in GPR15 expression (ß = 0.036, p = 4.86 × 10−5). Three novel GPR15 CpG sites were identified in relation to smoking and GPR15 expression. Our results provide novel insights in the regulation of GPR15, which possibly linked smoking to inflammation and disease progression. Full article
(This article belongs to the Special Issue Biomolecules for Translational Approaches in Cardiology)
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Open AccessArticle Intrinsic Iron Release Is Associated with Lower Mortality in Patients with Stable Coronary Artery Disease—First Report on the Prospective Relevance of Intrinsic Iron Release
Biomolecules 2018, 8(3), 72; https://doi.org/10.3390/biom8030072
Received: 9 July 2018 / Revised: 3 August 2018 / Accepted: 3 August 2018 / Published: 9 August 2018
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Abstract
Intrinsic iron release is discussed to have favorable effects in coronary artery disease (CAD). The aim of this study was to evaluate the prognostic relevance of intrinsic iron release in patients with CAD. Intrinsic iron release was based on a definition including hepcidin
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Intrinsic iron release is discussed to have favorable effects in coronary artery disease (CAD). The aim of this study was to evaluate the prognostic relevance of intrinsic iron release in patients with CAD. Intrinsic iron release was based on a definition including hepcidin and soluble transferrin receptor (sTfR). In a cohort of 811 patients with angiographically documented CAD levels of hepcidin and sTfR were measured at baseline. Systemic body iron release was defined as low levels of hepcidin (<24 ng/mL) and high levels of sTfR (≥2 mg/L). A commercially available ELISA (DRG) was used for measurements of serum hepcidin. Serum sTfR was determined by using an automated immunoassay (). Cardiovascular mortality was the main outcome measure. The criteria of intrinsic iron release were fulfilled in 32.6% of all patients. Significantly lower cardiovascular mortality rates were observed in CAD patients with systemic iron release. After adjustment for body mass index, smoking status, hypertension, diabetes, dyslipidemia, sex, and age, the hazard ratio for future cardiovascular death was 0.41. After an additional adjustment for surrogates of the size of myocardial necrosis (troponin I), anemia (hemoglobin), and cardiac function and heart failure severity (N-terminal pro B-type natriuretic peptide), this association did not change (Hazard ratio 0.37 (95% confidence interval 0.14–0.99), p = 0.047). In conclusion, significantly lower cardiovascular mortality rates were observed in CAD patients with intrinsic iron release shown during follow-up. Full article
(This article belongs to the Special Issue Biomolecules for Translational Approaches in Cardiology)
Open AccessArticle Low-Circulating Homoarginine is Associated with Dilatation and Decreased Function of the Left Ventricle in the General Population
Biomolecules 2018, 8(3), 63; https://doi.org/10.3390/biom8030063
Received: 1 June 2018 / Revised: 10 July 2018 / Accepted: 19 July 2018 / Published: 30 July 2018
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Abstract
Low homoarginine is an independent marker of mortality in heart failure patients and incident cardiovascular events. Whether homoarginine is related with healthier cardiac structure and function is currently unclear. We used data of the population-based “Study of Health in Pomerania” (SHIP-Trend) to assess
[...] Read more.
Low homoarginine is an independent marker of mortality in heart failure patients and incident cardiovascular events. Whether homoarginine is related with healthier cardiac structure and function is currently unclear. We used data of the population-based “Study of Health in Pomerania” (SHIP-Trend) to assess this relation. Homoarginine was measured in serum using liquid chromatography-tandem mass spectrometry. Linear regression models assessed the relation between homoarginine and several structural as well as functional parameters and N-terminal pro B-type natriuretic peptide (NTproBNP). All models were adjusted for age, sex, body mass index, and renal function. A total of 3113 subjects (median age 48 (25th percentile 37 to 75th percentile 60) years, 46% male) were included. A standard deviation decrease in homoarginine was associated with a larger left ventricular diastolic diameter (0.3; 95%-confidence interval (CI): 0.2 to 0.5 mm; p < 0.001), left ventricular systolic diameter (0.38; 95%-CI: −0.22 to 0.54 mm; p < 0.001) as well as a less relative wall thickness (–0.003 95%-CI: −0.006 to −0.0008; p = 0.01), left ventricular ejection fraction (–0.47; 95%-CI: –0.79 to −0.15%; p < 0.01) and fractional shortening (−0.35; 95%-CI: −0.62 to 0.07%; p = 0.01). Low homoarginine was also related to higher NTproBNP (−0.02 95%-CI: −0.034 to −0.009 log pg/mL; p < 0.01). Lower serum homoarginine is associated with dilatation of the heart and decreased function. Prospective clinical studies should assess if homoarginine supplementation improves cardiac health in subjects with low serum concentrations. Full article
(This article belongs to the Special Issue Biomolecules for Translational Approaches in Cardiology)
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Open AccessArticle Adverse Outcome Prediction of Iron Deficiency in Patients with Acute Coronary Syndrome
Biomolecules 2018, 8(3), 60; https://doi.org/10.3390/biom8030060
Received: 8 June 2018 / Revised: 9 July 2018 / Accepted: 16 July 2018 / Published: 20 July 2018
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Abstract
Acute myocardial infarction remains a leading cause of morbidity and mortality. While iron deficient heart failure patients are at increased risk of future cardiovascular events and see improvement with intravenous supplementation, the clinical relevance of iron deficiency in acute coronary syndrome remains unclear.
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Acute myocardial infarction remains a leading cause of morbidity and mortality. While iron deficient heart failure patients are at increased risk of future cardiovascular events and see improvement with intravenous supplementation, the clinical relevance of iron deficiency in acute coronary syndrome remains unclear. We aimed to evaluate the prognostic value of iron deficiency in the acute coronary syndrome (ACS). Levels of ferritin, iron, and transferrin were measured at baseline in 836 patients with ACS. A total of 29.1% was categorized as iron deficient. The prevalence of iron deficiency was clearly higher in women (42.8%), and in patients with anemia (42.5%). During a median follow-up of 4.0 years, 111 subjects (13.3%) experienced non-fatal myocardial infarction (MI) and cardiovascular mortality as combined endpoint. Iron deficiency strongly predicted non-fatal MI and cardiovascular mortality with a hazard ratio (HR) of 1.52 (95% confidence interval (CI) 1.03-2.26; p = 0.037) adjusted for age, sex, hypertension, smoking status, diabetes, hyperlipidemia, body-mass-index (BMI) This association remained significant (HR 1.73 (95% CI 1.07–2.81; p = 0.026)) after an additional adjustment for surrogates of cardiac function and heart failure severity (N-terminal pro B-type natriuretic peptide, NT-proBNP), for the size of myocardial necrosis (troponin), and for anemia (hemoglobin). Survival analyses for cardiovascular mortality and MI provided further evidence for the prognostic relevance of iron deficiency (HR 1.50 (95% CI 1.02–2.20)). Our data showed that iron deficiency is strongly associated with adverse outcome in acute coronary syndrome. Full article
(This article belongs to the Special Issue Biomolecules for Translational Approaches in Cardiology)
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Open AccessCommunication A Novel Class of tRNA-Derived Small Non-Coding RNAs Respond to Myocardial Hypertrophy and Contribute to Intergenerational Inheritance
Biomolecules 2018, 8(3), 54; https://doi.org/10.3390/biom8030054
Received: 14 April 2018 / Revised: 12 June 2018 / Accepted: 9 July 2018 / Published: 16 July 2018
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Abstract
tRNA-derived fragments (tRFs) are a new class of non-coding RNA that play an important role in regulating cellular RNA processing and protein translation. However, there is currently no study reporting the influence of tRFs on myocardial hypertrophy. In this study, we used an
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tRNA-derived fragments (tRFs) are a new class of non-coding RNA that play an important role in regulating cellular RNA processing and protein translation. However, there is currently no study reporting the influence of tRFs on myocardial hypertrophy. In this study, we used an isoproterenol (ISO)-induced myocardial hypertrophy rat model. Small RNA (<40 nts) transcriptome sequencing was used to select differentially expressed tRFs. We also compared the tRFs expression pattern in F0 sperm and the hearts of F1 offspring between the myocardial hypertrophy group (Hyp) and the control group (Con). Isoproterenol successfully induced a typical cardiac hypertrophy model in our study. Small RNA-seq revealed that tRFs were extremely enriched (84%) in the Hyp heart. Overexpression of tRFs1 and tRFs2 both enlarged the surface area of cardiac cells and increased expression of hypertrophic markers (ANF, BNP, and β-MHC). Luciferase reporter assay identified that tRFs1 directly target 3′UTR of Timp3. tRFs1, tRFs2, tRFs3, and tRFs4 were also highly expressed in Hyp F0 sperm and in Hyp F1 offspring hearts, but there was no differential expression of tRFs7, tRFs9, and tRFs10. Compared to Con F1 offspring, Hyp F1 offspring had elevated expression levels of β-MHC and ANP genes, and they had increased fibrosis and apoptosis in their hearts. These results demonstrated that tRFs are involved in regulating the response of myocardial hypertrophy. Besides, tRFs might serve as novel epigenetic factors that contribute to the intergenerational inheritance of cardiac hypertrophy. Full article
(This article belongs to the Special Issue Biomolecules for Translational Approaches in Cardiology)
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Open AccessArticle Prognostic Value of Iron-Homeostasis Regulating Peptide Hepcidin in Coronary Heart Disease—Evidence from the Large AtheroGene Study
Biomolecules 2018, 8(3), 43; https://doi.org/10.3390/biom8030043
Received: 8 June 2018 / Revised: 25 June 2018 / Accepted: 26 June 2018 / Published: 28 June 2018
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Abstract
Iron is essential in terms of oxygen utilization and mitochondrial function. The liver-derived peptide hepcidin has been recognized as a key regulator of iron homeostasis. Since iron metabolism is crucially linked to cardiovascular health, and low hepcidin was proposed as potential new marker
[...] Read more.
Iron is essential in terms of oxygen utilization and mitochondrial function. The liver-derived peptide hepcidin has been recognized as a key regulator of iron homeostasis. Since iron metabolism is crucially linked to cardiovascular health, and low hepcidin was proposed as potential new marker of iron metabolism, we aimed to evaluate the prognostic value of hepcidin in a large cohort of patients with coronary heart disease (CHD). Serum levels of hepcidin were determined at baseline in patients with angiographically documented CHD. The main outcome measure was non-fatal myocardial infarction (MI) or cardiovascular death. During a median follow-up of 4.1 years, 10.3% experienced an endpoint. In Cox regression analyses for hepcidin the hazard ratio for future cardiovascular death or MI was 1.03 (95% confidence interval (CI) 0.91–1.18, p = 0.63) after adjustment for sex and age. This association virtually did not change after additional adjustment for body mass index (BMI), smoking status, hypertension, diabetes, dyslipidemia, and surrogates of cardiac function (NT-proBNP), size of myocardial necrosis (troponin I), and anemia (hemoglobin). In this study, by far the largest evaluating the predictive value of hepcidin, hepcidin levels were not associated with future MI or cardiovascular death. This implicates a limited, if any, role for hepcidin in secondary cardiovascular risk prediction. Full article
(This article belongs to the Special Issue Biomolecules for Translational Approaches in Cardiology)
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Review

Jump to: Research

Open AccessReview Mineralocorticoid Receptor and Aldosterone-Related Biomarkers of End-Organ Damage in Cardiometabolic Disease
Biomolecules 2018, 8(3), 96; https://doi.org/10.3390/biom8030096
Received: 3 August 2018 / Revised: 10 September 2018 / Accepted: 12 September 2018 / Published: 18 September 2018
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Abstract
The mineralocorticoid receptor (MR) was first identified as a blood pressure regulator, modulating renal sodium handling in response to its principal ligand aldosterone. The mineralocorticoid receptor is also expressed in many tissues other than the kidney, such as adipose tissue, heart and vasculature.
[...] Read more.
The mineralocorticoid receptor (MR) was first identified as a blood pressure regulator, modulating renal sodium handling in response to its principal ligand aldosterone. The mineralocorticoid receptor is also expressed in many tissues other than the kidney, such as adipose tissue, heart and vasculature. Recent studies have shown that MR plays a relevant role in the control of cardiovascular and metabolic function, as well as in adipogenesis. Dysregulation of aldosterone/MR signaling represents an important cause of disease as high plasma levels of aldosterone are associated with hypertension, obesity and increased cardiovascular risk. Aldosterone displays powerful vascular effects and acts as a potent pro-fibrotic agent in cardiovascular remodeling. Mineralocorticoid receptor activation regulates genes involved in vascular and cardiac fibrosis, calcification and inflammation. This review focuses on the role of novel potential biomarkers related to aldosterone/MR system that could help identify cardiovascular and metabolic detrimental conditions, as a result of altered MR activation. Specifically, we discuss: (1) how MR signaling regulates the number and function of different subpopulations of circulating and intra-tissue immune cells; (2) the role of aldosterone/MR system in mediating cardiometabolic diseases induced by obesity; and (3) the role of several MR downstream molecules as novel potential biomarkers of cardiometabolic diseases, end-organ damage and rehabilitation outcome. Full article
(This article belongs to the Special Issue Biomolecules for Translational Approaches in Cardiology)
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Open AccessReview Potential Impact of Oral Inflammations on Cardiac Functions and Atrial Fibrillation
Biomolecules 2018, 8(3), 66; https://doi.org/10.3390/biom8030066
Received: 21 June 2018 / Revised: 14 July 2018 / Accepted: 26 July 2018 / Published: 1 August 2018
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Abstract
Inflammation may be a risk factor for atrial fibrillation (AF). Oral infections frequently lead to chronic inflammation, such as gingivitis, periodontitis, and endodontic lesions. In this narrative review, we consider five basic pathogenic mechanisms that involve oral infections and inflammations in the pathogenesis
[...] Read more.
Inflammation may be a risk factor for atrial fibrillation (AF). Oral infections frequently lead to chronic inflammation, such as gingivitis, periodontitis, and endodontic lesions. In this narrative review, we consider five basic pathogenic mechanisms that involve oral infections and inflammations in the pathogenesis of AF: (1) low level bacteremia by which oral bacteria enter the blood stream at inflamed sites of the oral cavity and invade the heart; (2) Systemic inflammation induced by inflammatory mediators, which are released from the sites of oral inflammation into the blood stream, affecting cardiac remodeling; (3) autoimmunity against molecular structures expressed in the heart caused by the host immune response to specific components of oral pathogens; (4) potentially arrhythmic effects mediated by activation of the autonomous nervous system triggered by oral inflammations; and (5) arrhythmic effects resulting from specific bacterial toxins that are produced by oral pathogenic bacteria. A number of studies support the involvement of all five mechanisms, suggesting a potentially complex contribution of oral inflammations to the pathogenesis of AF. Full article
(This article belongs to the Special Issue Biomolecules for Translational Approaches in Cardiology)
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Open AccessFeature PaperReview Novel Approaches for BAV Aortopathy Prediction—Is There a Need for Cohort Studies and Biomarkers?
Biomolecules 2018, 8(3), 58; https://doi.org/10.3390/biom8030058
Received: 30 May 2018 / Revised: 9 July 2018 / Accepted: 13 July 2018 / Published: 19 July 2018
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Abstract
Bicuspid aortic valve (BAV) disease is the most common congenital malformation of the human heart with a prevalence of 1–2% in the general population. More than half of patients with a BAV present with a dilated proximal aorta (so-called bicuspid aortopathy) which is
[...] Read more.
Bicuspid aortic valve (BAV) disease is the most common congenital malformation of the human heart with a prevalence of 1–2% in the general population. More than half of patients with a BAV present with a dilated proximal aorta (so-called bicuspid aortopathy) which is associated with an enhanced risk of life-threatening aortic complications. Up to now, the pathogenesis of bicuspid aortopathy as well as the risk stratification of aortic complications has not yet been sufficiently clarified. Recent findings have shown that bicuspid aortopathy features phenotypic heterogeneity. Two distinct valvulo-aortic phenotypes, the so-called root phenotype, as well as a dilation of the tubular ascending aorta, coincide with a significantly different risk for aortal complications. However, the phenotype-based classification that is only based on these two clinical forms is not sufficient to estimate the risk of aortal complications in a prognostically relevant way. Therefore, there is growing clinical interest to assess novel approaches in BAV research and to introduce circulating biomarkers as an elegant diagnostic tool to improve risk stratification in BAV aortopathy. A large scale epidemiological cohort study, ranking from apparently healthy individuals to disease patients, and comprehensive biobanks provide the opportunity to study BAV disease and its complications and to identify novel biomarkers for BAV aortopathy surveillance and prognosis. Firstly, the data indicate that several protein-based biomarkers and non-coding RNA molecules, in particular circulating microRNAs, can serve as relevant molecular biomarkers to predict the course of BAV-associated aortopathy. Here, we review the current literature and knowledge about BAV from a clinical point of view, and report about novel approaches in BAV biomarker research. Full article
(This article belongs to the Special Issue Biomolecules for Translational Approaches in Cardiology)
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Open AccessFeature PaperReview Nontraditional Cardiovascular Biomarkers and Risk Factors: Rationale and Future Perspectives
Biomolecules 2018, 8(2), 40; https://doi.org/10.3390/biom8020040
Received: 15 May 2018 / Revised: 11 June 2018 / Accepted: 13 June 2018 / Published: 15 June 2018
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Abstract
The primary prevention of cardiovascular (CV) disease depends on the capacity to identify subjects at higher risk long before the occurrence of CV clinical manifestations. Traditional risk factors do not cover fully prediction of individual risk. Moreover, there is an area of gray
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The primary prevention of cardiovascular (CV) disease depends on the capacity to identify subjects at higher risk long before the occurrence of CV clinical manifestations. Traditional risk factors do not cover fully prediction of individual risk. Moreover, there is an area of gray for patients at intermediate CV risk, which offers wide margins of improvement. These observations highlight the need for new additive tools for a more accurate risk stratification. An increasing number of candidate biomarkers have been identified to predict CV risk and events, although they generally give only a moderate increase when added to currently available predictive scores. The approach utilizing a relative small number of biomarkers in multiple combinations, but only weakly related to each other or unrelated, thus belonging to independent-pathways, and so able to catch the multidimensional characteristic of atherosclerosis, appears promising. We discuss vitamin D and bone turnover biomarkers, hepatitis C virus, and psycho-emotional factors that may reflect alternative pathways over those generally considered for atherosclerosis (e.g., aspects directly related to inflammation and thrombosis). These new biomarkers could facilitate a more accurate assessment of CV risk stratification if incorporated in the current risk assessment algorithms. Full article
(This article belongs to the Special Issue Biomolecules for Translational Approaches in Cardiology)
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