Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.3
5.5
Journals
Biomolecules
Special Issues
Calcification in Cardiovascular Disease
share announcement

Calcification in Cardiovascular Disease

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

Deadline for manuscript submissions: closed (16 September 2022) | Viewed by 9237

Special Issue Editors

Prof. Dr. Inês Falcão Pires

E-Mail Website
Guest Editor
UnIC - Cardiovascular Research & Development Centre, Department of Surgery and Physiology, Faculty of Medicine, University of Porto, Alameda Prof. Hernâni Monteiro, 4200-319 Porto, Portugal
Interests: aortic valve stenosis; myocardial remodelling; reverse remodelling; myocardial metabolism
Dr. Laura Mouriño-Alvarez

E-Mail Website
Guest Editor
Department of Vascular Physiopathology, Hospital Nacional de Parapléjicos, SESCAM, 45071 Toledo, Spain
Interests: aortic stenosis; cardiovascular diseases; proteomics; molecular biology; cardiovascular risk factors
Dr. Fábio Trindade

E-Mail Website
Guest Editor
UnIC - Cardiovascular Research & Development Centre, Department of Surgery and Physiology, Faculty of Medicine, University of Porto, Alameda Prof. Hernâni Monteiro, 4200-319 Porto, Portugal
Interests: aortic stenosis; cardiovascular diseases; proteins; peptides; proteomics; bioinformatics

Special Issue Information

Dear Colleagues,

Calcification is a highly regulated phenomenon in the human body, with mineralization being promoted at specific sites, such as bones, and inhibited at soft tissues, such as in myocardium or in vessels. Under pathological conditions though, resulting from inflammatory reactions, metabolic disarrangements or even due to the natural aging course, unwanted calcification of, among others, cardiovascular tissues, from arteries to myocardium and heart valves, ensues. A natural consequence of calcification is the stiffening of the tissues, resulting in cardiovascular loss-of-function and greatly increasing the risk for many diseases, namely, coronary artery disease, peripheral artery disease, aortic stenosis, mitral stenosis, and for cardiovascular mortality. We lack a complete understanding of the pathways and players underlying pathological cardiovascular calcification, and we still need to implement biomarkers thereof in the clinical setting. We thus welcome submissions of original papers and reviews covering all aspects of calcification in cardiovascular disease (heart and vessels), following basic and translational approaches, ultimately contributing to a better understanding of the molecular and cellular regulation of pathological calcium deposition and to the clinical relevance of this pernicious phenomenon.

Prof. Dr. Inês Falcão Pires
Dr. Laura Mouriño-Alvarez
Dr. Fábio Trindade
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. Biomolecules is an international peer-reviewed open access monthly 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

  • calcification
  • cardiovascular disease
  • biomarkers
  • heart
  • vessels

Published Papers (4 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

14 pages, 2994 KiB  
Article
Periostin Augments Vascular Smooth Muscle Cell Calcification via β-Catenin Signaling
by Ioana Alesutan, Laura A. Henze, Beate Boehme, Trang T. D. Luong, Daniel Zickler, Burkert Pieske, Kai-Uwe Eckardt, Andreas Pasch and Jakob Voelkl
Biomolecules 2022, 12(8), 1157; https://doi.org/10.3390/biom12081157 - 21 Aug 2022
Cited by 6 | Viewed by 2141
Abstract
Medial vascular calcification is common in chronic kidney disease (CKD) and is closely linked to hyperphosphatemia. Vascular smooth muscle cells (VSMCs) can take up pro-calcific properties and actively augment vascular calcification. Various pro-inflammatory mediators are able to promote VSMC calcification. In this study, [...] Read more.
Medial vascular calcification is common in chronic kidney disease (CKD) and is closely linked to hyperphosphatemia. Vascular smooth muscle cells (VSMCs) can take up pro-calcific properties and actively augment vascular calcification. Various pro-inflammatory mediators are able to promote VSMC calcification. In this study, we investigated the effects and mechanisms of periostin, a matricellular signaling protein, in calcifying human VSMCs and human serum samples. As a result, periostin induced the mRNA expression of pro-calcific markers in VSMCs. Furthermore, periostin augmented the effects of β-glycerophosphate on the expression of pro-calcific markers and aggravated the calcification of VSMCs. A periostin treatment was associated with an increased β-catenin abundance as well as the expression of target genes. The pro-calcific effects of periostin were ameliorated by WNT/β-catenin pathway inhibitors. Moreover, a co-treatment with an integrin αvβ3-blocking antibody blunted the pro-calcific effects of periostin. The silencing of periostin reduced the effects of β-glycerophosphate on the expression of pro-calcific markers and the calcification of VSMCs. Elevated serum periostin levels were observed in hemodialysis patients compared with healthy controls. These observations identified periostin as an augmentative factor in VSMC calcification. The pro-calcific effects of periostin involve integrin αvβ3 and the activation of the WNT/β-catenin pathway. Thus, the inhibition of periostin may be beneficial to reduce the burden of vascular calcification in CKD patients. Full article
(This article belongs to the Special Issue Calcification in Cardiovascular Disease)
►▼ Show Figures

Figure 1

16 pages, 2249 KiB  
Article
Vascular Calcification and the Gut and Blood Microbiome in Chronic Kidney Disease Patients on Peritoneal Dialysis: A Pilot Study
by Ana Merino-Ribas, Ricardo Araujo, Luciano Pereira, Joana Campos, Luísa Barreiros, Marcela A. Segundo, Nádia Silva, Carolina F. F. A. Costa, Janete Quelhas-Santos, Fábio Trindade, Inês Falcão-Pires, Ines Alencastre, Ioana Bancu Dumitrescu and Benedita Sampaio-Maia
Biomolecules 2022, 12(7), 867; https://doi.org/10.3390/biom12070867 - 21 Jun 2022
Cited by 14 | Viewed by 2894
Abstract
Vascular calcification (VC) is a frequent condition in chronic kidney disease (CKD) and a well-established risk factor for the development of cardiovascular disease (CVD). Gut dysbiosis may contribute to CVD and inflammation in CKD patients. Nonetheless, the role of gut and blood microbiomes [...] Read more.
Vascular calcification (VC) is a frequent condition in chronic kidney disease (CKD) and a well-established risk factor for the development of cardiovascular disease (CVD). Gut dysbiosis may contribute to CVD and inflammation in CKD patients. Nonetheless, the role of gut and blood microbiomes in CKD-associated VC remains unknown. Therefore, this pilot study aimed to explore the link between gut and blood microbiomes and VC in CKD patients on peritoneal dialysis (CKD-PD). Our results showed relative changes in specific taxa between CKD-PD patients with and without VC, namely Coprobacter, Coprococcus 3, Lactobacillus, and Eubacterium eligens group in the gut, and Cutibacterium, Pajaroellobacter, Devosia, Hyphomicrobium, and Pelomonas in the blood. An association between VC and all-cause mortality risk in CKD-PD patients was also observed, and patients with higher mortality risk corroborate the changes of Eubacterium eligens in the gut and Devosia genus in the blood. Although we did not find differences in uremic toxins, intestinal translocation markers, and inflammatory parameters among CKD-PD patients with and without VC, soluble CD14 (sCD14), a nonspecific marker of monocyte activation, positively correlated with VC severity. Therefore, gut Eubacterium eligens group, blood Devosia, and circulating sCD14 should be further explored as biomarkers for VC, CVD, and mortality risk in CKD. Full article
(This article belongs to the Special Issue Calcification in Cardiovascular Disease)
►▼ Show Figures

Figure 1

14 pages, 1739 KiB  
Article
Osteoprotegerin Is a Better Predictor for Cardiovascular and All-Cause Mortality than Vascular Calcifications in a Multicenter Cohort of Patients on Peritoneal Dialysis
by Marcela Ávila, Ma. del Carmen Prado, Renata Romero, Ricardo Córdova, Ma. del Carmen Rigo, Miguel Trejo, Carmen Mora, Ramón Paniagua and for the Mexican Nephrology Collaborative Study Group
Biomolecules 2022, 12(4), 551; https://doi.org/10.3390/biom12040551 - 08 Apr 2022
Cited by 5 | Viewed by 1743
Abstract
The purpose of this study was to compare vascular calcification (VC), serum osteoprotegerin (OPG) levels, and other biochemical markers to determine their value as available predictors of all-cause and cardiovascular (CV) mortality in patients on peritoneal dialysis (PD). A total of 197 patients [...] Read more.
The purpose of this study was to compare vascular calcification (VC), serum osteoprotegerin (OPG) levels, and other biochemical markers to determine their value as available predictors of all-cause and cardiovascular (CV) mortality in patients on peritoneal dialysis (PD). A total of 197 patients were recruited from seven dialysis centers in Mexico City. VC was assessed with multi-slice computed tomography, measured using the calcification score (CaSc). OPG, albumin, calcium, hsC-reactive protein, phosphorous, osteocalcin, total alkaline phosphatase, and intact parathormone were also analyzed. Follow-up and mortality analyses were assessed using the Cox regression model. The mean age was 43.9 ± 12.9 years, 64% were males, and 53% were diabetics. The median OPG was 11.28 (IQR: 7.6–17.4 pmol/L), and 42% of cases had cardiovascular calcifications. The median VC was 424 (IQR:101–886). During follow-up (23 ± 7 months), there were 34 deaths, and 44% were cardiovascular in origin. In multivariable analysis, OPG was a significant predictor for all-cause (HR 1.08; p < 0.002) and CV mortality (HR 1.09; p < 0.013), and performed better than VC (HR 1.00; p < 0.62 for all-cause mortality and HR 1.00; p < 0.16 for CV mortality). For each mg/dL of albumin-corrected calcium, there was an increased risk for CV mortality, and each g/dL of albumin decreased the risk factor for all-cause mortality. OPG levels above 14.37 and 13.57 pmol/L showed the highest predictive value for all-cause and CV mortality in incident PD patients and performed better than VC. Full article
(This article belongs to the Special Issue Calcification in Cardiovascular Disease)
►▼ Show Figures

Figure 1

11 pages, 1854 KiB  
Article
Longitudinal Effects of Serum Calcium and Phosphate Levels and Their Ratio on Incident Ischemic Heart Disease among Korean Adults
by Dong Hyuk Jung, Byoungjin Park and Yong Jae Lee
Biomolecules 2022, 12(1), 103; https://doi.org/10.3390/biom12010103 - 08 Jan 2022
Cited by 6 | Viewed by 1724
Abstract
Serum calcium and phosphate levels are controlled by a regulatory system, but their individual concentration tendencies and interactions may affect long-term vascular health. This study aimed to assess the effects of serum calcium and phosphate levels on incident ischemic heart disease (IHD) in [...] Read more.
Serum calcium and phosphate levels are controlled by a regulatory system, but their individual concentration tendencies and interactions may affect long-term vascular health. This study aimed to assess the effects of serum calcium and phosphate levels on incident ischemic heart disease (IHD) in a large-scale community-dwelling Korean cohort. We evaluated 15,259 non-diabetic individuals (median age, 45 years; range, 30–85) without previous IHD or ischemic stroke using the Korean National Health Insurance data. The study population was classified based on the calcium, phosphate, and calcium/phosphate ratios. Using Cox proportional hazards regression models, we estimated hazard ratios (HRs) with 95% confidence intervals (CIs) for IHD over 50 months after baseline enrolment. The age- and sex-adjusted incidence of IHD gradually increased with serum calcium and phosphate quartiles and decreased with calcium/phosphate ratio quartiles, with an overall crude rate of 2.1% (315/15,259). After setting the lowest calcium, phosphate, and calcium/phosphate ratio quartiles as a reference group, the HRs (95% CIs) of the highest calcium, phosphate, and calcium/phosphate ratio quartiles for IHD were 1.77 (1.15–2.72), 1.73 (1.18–2.55), and 0.58 (0.39–0.87), respectively, after adjusting for potential confounding variables. Serum calcium and phosphate levels were positively associated with IHD incidence, while the serum calcium/phosphate ratio exhibited an inverse relationship. Serum calcium and phosphate homeostasis may merit serious consideration to understand the pathogenesis of coronary atherosclerosis as a risk modifier for IHD. Full article
(This article belongs to the Special Issue Calcification in Cardiovascular Disease)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-4
Back to TopTop