Classical and Novel Biomarkers for Cardiovascular Disease

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biomarkers".

Deadline for manuscript submissions: closed (31 March 2023) | Viewed by 6359

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Guest Editor
José Ferro Lab—Clinical Research in Non-Communicable Neurological Diseases, Instituto de Medicina Molecular João Lobo Antunes, Faculdade de Medicina, Universidade de Lisboa, 1649-028 Lisbon, Portugal
Interests: stroke; biomarkers; precision medicine; cardioembolism
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Special Issue Information

Dear Colleagues,

Cardiovascular and cerebrovascular diseases are still among the major causes of morbidity and mortality worldwide. Lifestyle risk factors such as smoking, diet, obesity and physical inactivity contribute to increase the incidence of cardiovascular events by promoting a proinflammatory condition that affects the proliferation, migration and increased permeability of endothelial cells. In turn, the endothelial inflammatory phenotype triggers the synthesis and release of cytokines, chemokines and growth factors that further exacerbate endothelial health and impair vascular performance. However, searching for biological markers able to evaluate cardiovascular diseases is still a great challenge.

Among the most validated biomarkers that are currently in use, inflammation-related markers are prominent. Some classical and novel biomarkers have emerged as relevant contributors in the energy-homeostasis field, and have appeared as valid biomarkers of various cardiovascular and metabolic diseases. Among these presumed and specific biomarkers, several members of the TGF-beta super-family, GDF15, GDF11, newly emerging cardiokines, miRNAs, and markers discovered via proteomics in relation to oxidative stress are involved in cardiovascular disease. The evaluation of their circulating levels might provide new insights into the course of the disease. Finally, classical and novel biomarkers can also serve as new diagnostic markers for the detection of cardiovascular disorders to guide prognostication and emerging therapeutics. Authors are invited to submit original articles and review manuscripts addressing the topic of this Special Issue.

Dr. Ana Catarina Fonseca
Guest Editor

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Keywords

  • biomarkers
  • cardiovascular disease
  • cerebrovascular disease
  • cardiovascular therapy
  • diagnosis

Published Papers (4 papers)

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Research

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13 pages, 1571 KiB  
Article
Association of Long Noncoding RNA Expression Signatures with Stress-Induced Myocardial Perfusion Defects
by Yu-Chieh Chang, Jun-Ting Liou, Yu-Min Peng, Guan-Jun Chen, Chien-Yu Lin and Chin-An Yang
Biomolecules 2023, 13(5), 849; https://doi.org/10.3390/biom13050849 - 17 May 2023
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Abstract
Stress-induced myocardial perfusion defects found in dipyridamole–thallium-201 single-photon emission computed tomography imaging may indicate vascular perfusion abnormalities and risk of obstructive or nonobstructive coronary heart disease. Besides nuclear imaging and subsequent coronary angiography (CAG), no blood test can indicate whether dysregulated homeostasis is [...] Read more.
Stress-induced myocardial perfusion defects found in dipyridamole–thallium-201 single-photon emission computed tomography imaging may indicate vascular perfusion abnormalities and risk of obstructive or nonobstructive coronary heart disease. Besides nuclear imaging and subsequent coronary angiography (CAG), no blood test can indicate whether dysregulated homeostasis is associated with stress-induced myocardial perfusion defects. This study investigated the expression signature of long noncoding RNAs (lncRNAs) and genes involved in vascular inflammation and stress response in the blood of patients with stress-induced myocardial perfusion abnormalities (n = 27). The results revealed an expression signature consisting of the upregulation of RMRP (p < 0.01) and downregulations of THRIL (p < 0.01) and HIF1A (p < 0.01) among patients with a positive thallium stress test and no significant coronary artery stenosis within 6 months after baseline treatment. We developed a scoring system based on the expression signatures of RMRP, MIAT, NTT, MALAT1, HSPA1A, and NLRP3 to predict the need for further CAG among patients with moderate-to-significant stress-induced myocardial perfusion defects (area under the receiver operating characteristic curve = 0.963). Therefore, we identified a dysregulated expression profile of lncRNA-based genes in the blood that could be valuable for the early detection of vascular homeostasis imbalance and personalized therapy. Full article
(This article belongs to the Special Issue Classical and Novel Biomarkers for Cardiovascular Disease)
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12 pages, 1172 KiB  
Article
The Beneficial Changes on Inflammatory and Endothelial Biomarkers Induced by Metabolic Surgery Decreases the Carotid Intima-Media Thickness in Men
by Pilar Cobeta, Roberto Pariente, Alvaro Osorio, Marta Marchan, Luis Blázquez, David Pestaña, Julio Galindo and José I. Botella-Carretero
Biomolecules 2022, 12(12), 1827; https://doi.org/10.3390/biom12121827 - 7 Dec 2022
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Abstract
Obesity increases cardiovascular risk in men through several mechanisms. Among them, low-grade chronic inflammation and obesity-associated hypogonadism have been described. We aimed to study the effects of metabolic surgery on the carotid-intima media thickness through changes in inflammatory, endothelial biomarkers, and testosterone. We [...] Read more.
Obesity increases cardiovascular risk in men through several mechanisms. Among them, low-grade chronic inflammation and obesity-associated hypogonadism have been described. We aimed to study the effects of metabolic surgery on the carotid-intima media thickness through changes in inflammatory, endothelial biomarkers, and testosterone. We included 60 men; 20 submitted to laparoscopic Roux-en-Y gastric bypass (RYGB), 20 to sleeve gastrectomy (SG), and 20 to lifestyle modification (controls). Several inflammatory and endothelial biomarkers and total testosterone (TT) were measured at baseline and six months after surgery. Free testosterone (FT) was calculated, and carotid intima-media thickness (cIMT) was measured by ultrasonography. Compared to controls, cIMT decreased after surgery concomitantly with CRP, PAI-1, sICAM-1, and IL-18 (p < 0.01) and with an increase in sTWEAK (p = 0.027), with no differences between RYGB and SG. The increase in TT and FT after surgery correlated with the changes in cIMT (p = 0.010 and p = 0.038, respectively), but this association disappeared after multivariate analysis. Linear regression showed that sTWEAK (ß = −0.245, p = 0.039), PAI-1 (ß = 0.346, p = 0.005), and CRP (ß = 0.236, p = 0.049) were associated with the changes in cIMT (R2 = 0.267, F = 6.664, p = 0.001). In conclusion, both RYGB and SG induced improvements in inflammation and endothelial biomarkers that drove a decrease in cIMT compared to men with obesity who submitted to diet and exercise. Full article
(This article belongs to the Special Issue Classical and Novel Biomarkers for Cardiovascular Disease)
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22 pages, 1608 KiB  
Article
Effects of One-Year Tofacitinib Therapy on Lipids and Adipokines in Association with Vascular Pathophysiology in Rheumatoid Arthritis
by Monika Czókolyová, Attila Hamar, Anita Pusztai, Gábor Tajti, Edit Végh, Zsófia Pethő, Nóra Bodnár, Ágnes Horváth, Boglárka Soós, Szilvia Szamosi, Anita Szentpéteri, Ildikó Seres, Mariann Harangi, György Paragh, György Kerekes, Levente Bodoki, Andrea Domján, Katalin Hodosi, Tamás Seres, György Panyi, Zoltán Szekanecz and Gabriella Szűcsadd Show full author list remove Hide full author list
Biomolecules 2022, 12(10), 1483; https://doi.org/10.3390/biom12101483 - 14 Oct 2022
Cited by 3 | Viewed by 1989
Abstract
Background: Cardiovascular (CV) morbidity, mortality and metabolic syndrome are associated with rheumatoid arthritis (RA). A recent trial has suggested increased risk of major CV events (MACE) upon the Janus kinase (JAK) inhibitor tofacitinib compared with anti-tumor necrosis factor α (TNF-α) therapy. In our [...] Read more.
Background: Cardiovascular (CV) morbidity, mortality and metabolic syndrome are associated with rheumatoid arthritis (RA). A recent trial has suggested increased risk of major CV events (MACE) upon the Janus kinase (JAK) inhibitor tofacitinib compared with anti-tumor necrosis factor α (TNF-α) therapy. In our study, we evaluated lipids and other metabolic markers in relation to vascular function and clinical markers in RA patients undergoing one-year tofacitinib therapy. Patients and methods: Thirty RA patients treated with either 5 mg or 10 mg bid tofacitinib were included in a 12-month follow-up study. Various lipids, paraoxonase (PON1), myeloperoxidase (MPO), thrombospondin-1 (TSP-1) and adipokine levels, such as adiponectin, leptin, resistin, adipsin and chemerin were determined. In order to assess flow-mediated vasodilation (FMD), common carotid intima-media thickness (IMT) and arterial pulse-wave velocity (PWV) ultrasonography were performed. Assessments were carried out at baseline, and 6 and 12 months after initiating treatment. Results: One-year tofacitinib therapy significantly increased TC, HDL, LDL, APOA, APOB, leptin, adipsin and TSP-1, while significantly decreasing Lp(a), chemerin, PON1 and MPO levels. TG, lipid indices (TC/HDL and LDL/HDL), adiponectin and resistin showed no significant changes. Numerous associations were found between lipids, adipokines, clinical markers and IMT, FMD and PWV (p < 0.05). Regression analysis suggested, among others, association of BMI with CRP and PWV (p < 0.05). Adipokines variably correlated with age, BMI, CRP, CCP, FMD, IMT and PWV, while MPO, PON1 and TSP-1 variably correlated with age, disease duration, BMI, RF and PWV (p < 0.05). Conclusions: JAK inhibition by tofacitinib exerts balanced effects on lipids and other metabolic markers in RA. Various correlations may exist between metabolic, clinical parameters and vascular pathophysiology during tofacitinib treatment. Complex assessment of lipids, metabolic factors together with clinical parameters and vascular pathophysiology may be utilized in clinical practice to determine and monitor the CV status of patients in relation with clinical response to JAK inhibition. Full article
(This article belongs to the Special Issue Classical and Novel Biomarkers for Cardiovascular Disease)
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Review

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11 pages, 666 KiB  
Review
Update on Biomarkers Associated with Large-Artery Atherosclerosis Stroke
by Madalena Rosário and Ana Catarina Fonseca
Biomolecules 2023, 13(8), 1251; https://doi.org/10.3390/biom13081251 - 16 Aug 2023
Cited by 3 | Viewed by 1463
Abstract
Intracranial and extracranial large-artery atherosclerosis (LAA) are a main cause of ischemic stroke. Biomarkers may aid in the diagnosis of LAA and help to stratify patients’ risk of stroke. We performed a narrative review of the literature, mainly published in the last five [...] Read more.
Intracranial and extracranial large-artery atherosclerosis (LAA) are a main cause of ischemic stroke. Biomarkers may aid in the diagnosis of LAA and help to stratify patients’ risk of stroke. We performed a narrative review of the literature, mainly published in the last five years, with the aim of identifying biomarkers associated either with intracranial or extracranial LAA in humans. Several potential biomarkers of LAA, mainly related to lipidic pathways and inflammation, have been studied. Diagnostic biomarkers of LAA were evaluated by measuring biomarkers levels in patients with LAA stroke and other stroke etiologies. Some biomarkers were associated with the functional prognosis of LAA stroke patients. Increased levels of IL-6 and sLOX-1 were associated with a risk of progression of carotid atherosclerotic disease. Findings support the notion that the immune system plays a central role in the pathogenesis of LAA. Overall, in most studies, results were not externally validated. In the future, biomarkers could be useful for the selection of patients for clinical trials. To adopt these biomarkers in clinical practice, we will need robust multicentric studies proving their reproducibility and a clear practical applicability for their use. Full article
(This article belongs to the Special Issue Classical and Novel Biomarkers for Cardiovascular Disease)
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