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Cells
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Cardiovascular Biomarkers: Current Status and Future Directions
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Cardiovascular Biomarkers: Current Status and Future Directions

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Cardiovascular System".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 8076

Special Issue Editors

Dr. Markus M. Luedi

E-Mail Website
Guest Editor
Cantonal Hospital of St. Gallen, CH-9007 St. Gallen, Switzerland
Interests: biobanking; cardiovascular medicine; molecular biology; translational research; biomarkers
Special Issues, Collections and Topics in MDPI journals
Dr. Mark G. Filipovic

E-Mail Website
Guest Editor
Department of Anaesthesiology and Pain Medicine, Inselspital, Bern University Hospital, University of Bern, 3010 Bern, Switzerland
Interests: biobanking; cardiovascular medicine; molecular biology; translational research; biomarkers

Special Issue Information

Dear Colleagues,

After the initial increase in activity in genetic research in cardiovascular and perioperative medicine subsided due to the complexity and large cohorts that were required, the international research community put emphasis on biomarkers. These proteins are easy to analyze, often even in the routine laboratory, and have provided increasingly valuable data in recent years, especially in the acute care and perioperative setting. In cardiovascular medicine, in particular, we have gained a better understanding of how biomarkers can be effectively used for personalized risk analysis and outcome prediction purposes. In this Special Issue, we focus on the current status and future directions in cardiovascular biomarker research and invite the international community to submit carefully developed results from this research area.

Dr. Markus M. Luedi
Dr. Mark G. Filipovic
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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. Cells is an international peer-reviewed open access semimonthly 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 2700 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 medicine
  • biomarkers
  • translational research
  • outcome research
  • molecular biology
  • biobanking

Published Papers (4 papers)

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Editorial

Jump to: Research, Review

2 pages, 175 KiB  
Editorial
Cardiovascular Biomarkers: Current Status and Future Directions
by Mark G. Filipovic and Markus M. Luedi
Cells 2023, 12(22), 2647; https://doi.org/10.3390/cells12222647 - 17 Nov 2023
Viewed by 841
Abstract
Cardiovascular disease (CVD) remains a global health concern of paramount significance, claiming millions of lives each year [...] Full article
(This article belongs to the Special Issue Cardiovascular Biomarkers: Current Status and Future Directions)

Research

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17 pages, 2708 KiB  
Article
Circulated TGF-β1 and VEGF-A as Biomarkers for Fabry Disease-Associated Cardiomyopathy
by Margarita M. Ivanova, Julia Dao, Omar Abu Slayeh, Andrew Friedman and Ozlem Goker-Alpan
Cells 2023, 12(16), 2102; https://doi.org/10.3390/cells12162102 - 19 Aug 2023
Cited by 3 | Viewed by 1156
Abstract
Fabry disease (FD) is a lysosomal disorder caused by α-galactosidase A deficiency, resulting in the accumulation of globotriaosylceramide (Gb-3) and its metabolite globotriaosylsphingosine (Lyso-Gb-3). Cardiovascular complications and hypertrophic cardiomyopathy (HCM) are the most frequent manifestations of FD. While an echocardiogram and cardiac MRI [...] Read more.
Fabry disease (FD) is a lysosomal disorder caused by α-galactosidase A deficiency, resulting in the accumulation of globotriaosylceramide (Gb-3) and its metabolite globotriaosylsphingosine (Lyso-Gb-3). Cardiovascular complications and hypertrophic cardiomyopathy (HCM) are the most frequent manifestations of FD. While an echocardiogram and cardiac MRI are clinical tools to assess cardiac involvement, hypertrophic pattern variations and fibrosis make it crucial to identify biomarkers to predict early cardiac outcomes. This study aims to investigate potential biomarkers associated with HCM in FD: transforming growth factor-β1 (TGF-β1), TGF-β active form (a-TGF-β), vascular endothelial growth factor (VEGF-A), and fibroblast growth factor (FGF2) in 45 patients with FD, categorized into cohorts based on the HCM severity. TGF-β1, a-TGF-β, FGF2, and VEGF-A were elevated in FD. While the association of TGF-β1 with HCM was not gender-related, VEGF was elevated in males with FD and HCM. Female patients with abnormal electrocardiograms but without overt HCM also have elevated TGF-β1. Lyso-Gb3 is correlated with TGF-β1, VEGF-A, and a-TGF-β1. Elevation of TGF-β1 provides evidence of the chronic inflammatory state as a cause of myocardial fibrosis in FD patients; thus, it is a potential marker of early cardiac fibrosis detected even prior to hypertrophy. TGF-β1 and VEGF biomarkers may be prognostic indicators of adverse cardiovascular events in FD. Full article
(This article belongs to the Special Issue Cardiovascular Biomarkers: Current Status and Future Directions)
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14 pages, 2150 KiB  
Article
Ectodomain Shedding by ADAM17 Increases the Release of Soluble CD40 from Human Endothelial Cells under Pro-Inflammatory Conditions
by Anton Klersy, Sören Meyer, Florian Leuschner, Thorsten Kessler, Markus Hecker and Andreas H. Wagner
Cells 2023, 12(15), 1926; https://doi.org/10.3390/cells12151926 - 25 Jul 2023
Cited by 2 | Viewed by 4096
Abstract
Background: Homozygosity for the C allele of the −1T>C single nucleotide polymorphism (SNP) of the CD40 gene (rs1883832) is associated with susceptibility to coronary heart disease (CHD), enhanced CD40 expression, and shedding. The disintegrin metalloprotease ADAM17 can cleave various cell surface proteins. This [...] Read more.
Background: Homozygosity for the C allele of the −1T>C single nucleotide polymorphism (SNP) of the CD40 gene (rs1883832) is associated with susceptibility to coronary heart disease (CHD), enhanced CD40 expression, and shedding. The disintegrin metalloprotease ADAM17 can cleave various cell surface proteins. This study investigates an association between ADAM17-mediated CD40 shedding and inflammation in CC genotype human endothelial cells. Methods: Human umbilical vein endothelial cells (HUVEC) carrying the CC genotype were stimulated with soluble CD40 ligand (sCD40L) or tumor necrosis factor-α (TNFα). Messenger RNA and protein expression were determined with standard methods. Levels of high sensitive c-reactive protein (hs-CRP), interleukin-6 (IL-6), and sCD40 in plasma samples from patients with CHD were assessed using ELISA. Results: ADAM17 surface abundance was elevated following stimulation with CD40L and TNFα just as its regulator iRhom2. Inhibition of ADAM17 prevented TNFα-induced sCD40 and soluble vascular cell adhesion molecule-1 release into the conditioned medium and reinforced CD40 surface abundance. Secondary to inhibition of ADAM17, stimulation with CD40L or TNFα upregulated monocyte chemoattractant protein-1 mRNA and protein. Levels of sCD40 and the inflammatory biomarkers hs-CRP and IL-6 were positively correlated in the plasma of patients with CHD. Conclusions: We provide a mechanism by which membrane-bound CD40 is shed from the endothelial cell surface by ADAM17, boosting sCD40 formation and limiting downstream CD40 signaling. Soluble CD40 may represent a robust biomarker for CHD, especially in conjunction with homozygosity for the C allele of the −1T>C SNP of the CD40 gene. Full article
(This article belongs to the Special Issue Cardiovascular Biomarkers: Current Status and Future Directions)
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Review

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16 pages, 1780 KiB  
Review
The Role of FNDC5/Irisin in Cardiovascular Disease
by Maciej Grzeszczuk, Piotr Dzięgiel and Katarzyna Nowińska
Cells 2024, 13(3), 277; https://doi.org/10.3390/cells13030277 - 2 Feb 2024
Cited by 3 | Viewed by 1447
Abstract
Disorders of cardiomyocyte metabolism play a crucial role in many cardiovascular diseases, such as myocardial infarction, heart failure and ischemia–reperfusion injury. In myocardial infarction, cardiomyocyte metabolism is regulated by mitochondrial changes and biogenesis, which allows energy homeostasis. There are many proteins in cells [...] Read more.
Disorders of cardiomyocyte metabolism play a crucial role in many cardiovascular diseases, such as myocardial infarction, heart failure and ischemia–reperfusion injury. In myocardial infarction, cardiomyocyte metabolism is regulated by mitochondrial changes and biogenesis, which allows energy homeostasis. There are many proteins in cells that regulate and control metabolic processes. One of them is irisin (Ir), which is released from the transmembrane protein FNDC5. Initial studies indicated that Ir is a myokine secreted mainly by skeletal muscles. Further studies showed that Ir was also present in various tissues. However, its highest levels were observed in cardiomyocytes. Ir is responsible for many processes, including the conversion of white adipose tissue (WAT) to brown adipose tissue (BAT) by increasing the expression of thermogenin (UCP1). In addition, Ir affects mitochondrial biogenesis. Therefore, the levels of FNDC5/Ir in the blood and myocardium may be important in cardiovascular disease. This review discusses the current knowledge about the role of FNDC5/Ir in cardiovascular disease. Full article
(This article belongs to the Special Issue Cardiovascular Biomarkers: Current Status and Future Directions)
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