Submit to JPM Review for JPM Propose a Special Issue

Journal Menu

Journal Browser

Atherosclerosis: Technologies of Personalized Medicine

Print Special Issue Flyer
Special Issue Editors
Special Issue Information
Keywords
Benefits of Publishing in a Special Issue
Published Papers

A special issue of Journal of Personalized Medicine (ISSN 2075-4426). This special issue belongs to the section "Methodology, Drug and Device Discovery".

Deadline for manuscript submissions: closed (15 December 2021) | Viewed by 27461

Printed Edition Available!
A printed edition of this Special Issue is available here.

Special issue Atherosclerosis: Technologies of Personalized Medicine book cover image

Share This Special Issue

Special Issue Editor

Prof. Dr. Yuliya I. Ragino

E-Mail Website
Guest Editor

Institute of Internal and Preventive Medicine–Branch of Institute of Cytology and Genetics, Siberian Branch of Russian Academy of Sciences, 630089 Novosibirsk, Russia
Interests: key biochemical markers; the pathogenesis of metabolic syndrome and obesity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The worldwide prevalence of atherosclerosis and associated diseases is growing on an epidemic scale. Early detection of atherosclerotic changes requires modern molecular genetic, biochemical, pathophysiological, and equipment studies that enable personalized approaches to treatments.
Personalized medicine includes a range of approaches to health care based on factual data: from precise molecular diagnostics to prediction of the onset or development of disease based on genetic research.
We invite you to submit papers with the results of research on atherosclerosis aimed at improving technologies for the prevention, diagnosis, risk assessment, and treatment of atherosclerosis from the standpoint of personalized medicine.
In this Special Issue, original research articles and reviews are welcomed. Research areas may include (but not limited to) the following:

Experimental research in the field of atherosclerosis;
Biochemical studies on atherosclerosis;
Genomics, GWAS, and population genetics of atherosclerosis;
Atherosclerosis epigenetics and microRNAs;
Hereditary dyslipidemias;
Proteomic investigation of atherosclerosis;
Etiopathogenetic aspects of atherosclerosis;
Lipids, lipoproteins, and apolipoproteins;
Macrophages and atherosclerosis;
Vascular-wall remodeling and atherosclerosis;
Inflammation and atherosclerosis;
Oxidative stress and atherosclerosis;
Immunology of atherosclerosis;
Climatic-geographical and ethnic features of atherosclerosis development

We look forward to receiving your contributions.

Prof. Dr. Yuliya I. Ragino
Guest Editor

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. Journal of Personalized Medicine 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 2600 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

Atherosclerosis
Molecular genetic
Biochemical
Pathophysiological
Personalized medicine
Epigenetics
Cardiovascular disease

Benefits of Publishing in a Special Issue

Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (11 papers)

Download All Papers

Order results

Result details

Show export options Show export options

Select all

Export citation of selected articles as:

Editorial

Jump to: Research

4 pages, 182 KiB

Open AccessEditorial

Basic Research in Atherosclerosis: Technologies of Personalized Medicine

by Yuliya Ragino, Evgeniia Striukova and Elena Shakhtshneider

J. Pers. Med. 2022, 12(3), 367; https://doi.org/10.3390/jpm12030367 - 28 Feb 2022

Viewed by 1861

Abstract

The first national conference with international participation, “Fundamental aspects of atherosclerosis: scientific research for improving the technologies of personalized medicine”, was held in Novosibirsk on 15 October 2021 [...] Full article

(This article belongs to the Special Issue Atherosclerosis: Technologies of Personalized Medicine)

Research

Jump to: Editorial

13 pages, 1770 KiB

Open AccessArticle

Lipoprotein(a), Immune Cells and Cardiovascular Outcomes in Patients with Premature Coronary Heart Disease

by Olga I. Afanasieva, Alexandra V. Tyurina, Elena A. Klesareva, Tatiana I. Arefieva, Marat V. Ezhov and Sergei N. Pokrovsky

J. Pers. Med. 2022, 12(2), 269; https://doi.org/10.3390/jpm12020269 - 12 Feb 2022

Cited by 14 | Viewed by 2349

Abstract

The detection of lipoprotein(a) [Lp(a)] in the artery wall at the stage of lipid-bands formation may indicate that it participates in the atherosclerosis local nonspecific inflammatory process. Innate immune cells are involved in atherogenesis, with monocytes playing a major role in the initiation of atherosclerosis, while neutrophils can contribute to plaque destabilization. This work studies the relationship between Lp(a), immune blood cells and major adverse cardiovascular events (MACE) in patients with the early manifestation of coronary heart disease (CHD). The study included 200 patients with chronic CHD, manifested up to the age of 55 in men and 60 in women. An increased Lp(a) concentration [hyperLp(a)] was shown to predict cardiovascular events in patients with premature CHD with long-term follow-up. According to the logistic regression analysis results, an increase in the monocyte count with OR = 4.58 (95% CI 1.04–20.06) or lymphocyte-to-monocyte ratio with OR = 0.82 (0.68–0.99), (p < 0.05 for both) was associated with MACE in patients with early CHD, regardless of gender, age, classical risk factors, atherogenic lipoproteins concentration and statin intake. The combination of an increased monocyte count and hyperLp(a) significantly increased the proportion of patients with early CHD with subsequent development of MACE (p = 0.02, p_trend = 0.003). The odds of cardiovascular events in patients with early CHD manifestation were highest in patients with an elevated lymphocyte-to-monocyte ratio and an elevated Lp(a) level. A higher neutrophil blood count and an elevated neutrophil-to-lymphocyte ratio determined the faster development of MACE in patients with a high Lp(a) concentration. The data obtained in this study suggest that the high atherothrombogenicity of Lp(a) is associated with the “inflammatory” component and the innate immune cells involvement in this process. Thus, the easily calculated immunological ratios of blood cells and Lp(a) concentrations can be considered simple predictors of future cardiovascular events. Full article

(This article belongs to the Special Issue Atherosclerosis: Technologies of Personalized Medicine)

► Show Figures

Graphical abstract

10 pages, 884 KiB

Open AccessFeature PaperArticle

A Novel Integrated Biomarker for Evaluation of Risk and Severity of Coronary Atherosclerosis, and Its Validation

by Victoria A. Metelskaya, Natalia E. Gavrilova, Maria V. Zhatkina, Elena B. Yarovaya and Oxana M. Drapkina

J. Pers. Med. 2022, 12(2), 206; https://doi.org/10.3390/jpm12020206 - 2 Feb 2022

Cited by 8 | Viewed by 2111

Abstract

Objective: To assess the feasibility of a combination of biochemical and imaging parameters for estimation of risk and severity of coronary atherosclerosis (CA), and to verify the created integrated biomarker (i-BIO) on independent cohort. Methods: Two cohorts of patients admitted to the hospital for coronary angiography and ultrasound carotid dopplerography were enrolled into the study (n = 205 and n = 216, respectively). The extent of CA was assessed by Gensini Score (GS). Results: According to GS, participants were distributed as follows: atherosclerosis-free (GS = 0), CA of any stage (GS > 0), subclinical CA (GS < 35), severe CA (GS ≥ 35). Based on the analysis of mathematical models, including biochemical and imaging parameters, we selected and combined the most significant variables as i-BIO. The ability of i-BIO to detect the presence and severity of CA was estimated using ROC-analysis with cut-off points determination. Risk of any CA (GS > 0) at i-BIO > 4 was 7.3 times higher than in those with i-BIO ≤ 4; risk of severe CA (GS ≥ 35) at i-BIO ≥ 9 was 3.1 times higher than at i-BIO < 9. Results on the tested cohort confirmed these findings. Conclusions: The i-BIO > 4 detected CA (GS > 0) with sensitivity of 87.9%, i-BIO ≥ 9 excluded patients without severe CA (GS < 35), specificity 79.8%. Validation of i-BIO confirmed the feasibility of i-BIO > 4 to separate patients with any CA with sensitivity 76.2%, and of i-BIO ≥ 9 to exclude atherosclerosis-free subjects with specificity of 84.0%. Full article

(This article belongs to the Special Issue Atherosclerosis: Technologies of Personalized Medicine)

► Show Figures

Figure 1

17 pages, 1193 KiB

Open AccessArticle

Relationship between Epicardial and Coronary Adipose Tissue and the Expression of Adiponectin, Leptin, and Interleukin 6 in Patients with Coronary Artery Disease

by Olga V. Gruzdeva, Yulia A. Dyleva, Ekaterina V. Belik, Maxim Y. Sinitsky, Aleksandr N. Stasev, Aleksandr N. Kokov, Natalia K. Brel, Evgenia O. Krivkina, Evgenia E. Bychkova, Roman S. Tarasov and Olga L. Barbarash

J. Pers. Med. 2022, 12(2), 129; https://doi.org/10.3390/jpm12020129 - 19 Jan 2022

Cited by 24 | Viewed by 3074

Abstract

Adipose tissue (AT) is an endocrine and paracrine organ that synthesizes biologically active adipocytokines, which affect inflammation, fibrosis, and atherogenesis. Epicardial and perivascular fat depots are of great interest to researchers, owing to their potential effects on the myocardium and blood vessels. The aim of the study was to assess the expression and secretion of adipocytokine genes in the AT of patients with coronary artery disease (CAD) and patients with aortic or mitral valve replacement. This study included 84 patients with CAD and 50 patients with aortic or mitral valve replacement. Adipocytes were isolated from subcutaneous, epicardial (EAT), and perivascular AT (PVAT), and were cultured for 24 h. EAT exhibited the lowest level of adiponectin gene expression and secretion, regardless of nosology, and high expression levels of the leptin gene and interleukin-6 (IL-6). However, EAT adipocytes in patients with CAD were characterized by more pronounced changes in comparison with the group with heart defects. High leptin and IL-6 levels resulted in increased pro-inflammatory activity, as observed in both EAT and PVAT adipocytes, especially in individuals with CAD. Therefore, our results revealed the pathogenetic significance of alterations in the adipokine and cytokine status of adipocytes of EAT and PVAT in patients with CAD. Full article

(This article belongs to the Special Issue Atherosclerosis: Technologies of Personalized Medicine)

► Show Figures

Figure 1

12 pages, 1421 KiB

Open AccessFeature PaperArticle

The Determinants of the 13-Year Risk of Incident Atrial Fibrillation in a Russian Population Cohort of Middle and Elderly Age

by Marina Shapkina, Andrey Ryabikov, Ekaterina Mazdorova, Anastasia Titarenko, Ekaterina Avdeeva, Elena Mazurenko, Lilia Shcherbakova, Hynek Pikhart, Martin Bobak and Sofia Malyutina

J. Pers. Med. 2022, 12(1), 122; https://doi.org/10.3390/jpm12010122 - 17 Jan 2022

Cited by 4 | Viewed by 2432

Abstract

Atrial fibrillation (AF) is the most common arrhythmia and a predictor of the complications of atherosclerotic cardiovascular diseases (ASCVDs), particularly thromboembolic events and the progression of heart failure. We analyzed the determinants of the 13-year risk of incident AF in a Russian population cohort of middle and elderly age. A random population sample (n = 9360, age 45–69 years) was examined at baseline in 2003–2005 and reexamined in 2006–2008 and 2015–2017 in Novosibirsk (the HAPIEE study). Incident AF was being registered during the average follow-up of 13 years. The final analysis included 3871 participants free from baseline AF and cardiovascular disease (CVD) who participated in all three data collections. In a multivariable-adjusted Cox regression model, the 13-year risk of AF was positively associated with the male sex (hazard ratio (HR) = 2.20; 95% confidence interval (CI) 1.26–3.87); age (HR = 1.10 per year; 95% CI 1.07–1.14); body mass index (BMI), (HR = 1.11 per unit; 95% CI 1.07–1.15); systolic blood pressure (SBP), (HR = 1.02 per 1 mmHg; 95% CI 1.01–1.02), and it was negatively associated with total cholesterol (TC), (HR = 0.79 per 1 mmol/L; 95% CI 0.66–0.94). In women, the risk of AF was more strongly associated with hypertension (HT) and was also negatively related to total cholesterol (TC) level (HR = 0.74 per 1 mmol/L; 95% CI 0.56–0.96). No independent association was found with mean alcohol intake per drinking occasion. These results in a Russian cohort have an implication for the prediction of AF and ASCVD complications in the general population. Full article

(This article belongs to the Special Issue Atherosclerosis: Technologies of Personalized Medicine)

► Show Figures

Figure 1

14 pages, 1065 KiB

Open AccessArticle

The Relationship between Epigenetic Age and Myocardial Infarction/Acute Coronary Syndrome in a Population-Based Nested Case-Control Study

by Sofia Malyutina, Olga Chervova, Taavi Tillmann, Vladimir Maximov, Andrew Ryabikov, Valery Gafarov, Jaroslav A. Hubacek, Hynek Pikhart, Stephan Beck and Martin Bobak

J. Pers. Med. 2022, 12(1), 110; https://doi.org/10.3390/jpm12010110 - 14 Jan 2022

Cited by 7 | Viewed by 2569

Abstract

We investigated the relationship between ‘epigenetic age’ (EA) derived from DNA methylation (DNAm) and myocardial infarction (MI)/acute coronary syndrome (ACS). A random population sample was examined in 2003/2005 (n = 9360, 45–69, the HAPIEE project) and followed up for 15 years. From this cohort, incident MI/ACS (cases, n = 129) and age- and sex-stratified controls (n = 177) were selected for a nested case-control study. Baseline EA (Horvath’s, Hannum’s, PhenoAge, Skin and Blood) and the differences between EA and chronological age (CA) were calculated (ΔAHr, ΔAHn, ΔAPh, ΔASB). EAs by Horvath’s, Hannum’s and Skin and Blood were close to CA (median absolute difference, MAD, of 1.08, –1.91 and –2.03 years); PhenoAge had MAD of −9.29 years vs. CA. The adjusted odds ratios (ORs) of MI/ACS per 1–year increments of ΔAHr, ΔAHn, ΔASB and ΔAPh were 1.01 (95% CI 0.95–1.07), 1.01 (95% CI 0.95–1.08), 1.02 (95% CI 0.97–1.06) and 1.01 (0.93–1.09), respectively. When classified into tertiles, only the highest tertile of ΔAPh showed a suggestion of increased risk of MI/ACS with OR 2.09 (1.11–3.94) independent of age and 1.84 (0.99–3.52) in the age- and sex-adjusted model. Metabolic modulation may be the likely mechanism of this association. In conclusion, this case-control study nested in a prospective population-based cohort did not find strong associations between accelerated epigenetic age markers and risk of MI/ACS. Larger cohort studies are needed to re-examine this important research question. Full article

(This article belongs to the Special Issue Atherosclerosis: Technologies of Personalized Medicine)

► Show Figures

Figure 1

12 pages, 894 KiB

Open AccessArticle

The Role of Cumulative LDL Cholesterol in Cardiovascular Disease Development in Patients with Familial Hypercholesterolemia

by Victoria Korneva, Tatyana Kuznetsova and Ulrich Julius

J. Pers. Med. 2022, 12(1), 71; https://doi.org/10.3390/jpm12010071 - 7 Jan 2022

Cited by 8 | Viewed by 2138

Abstract

In patients with familial hypercholesterolemia (FH) the exposure of very high LDL-C concentration and cumulative LDL-C level (cum LDL-C) can play a significant role in the prognosis. Objective: to analyze the contribution of “cum LDL-C for all life” and the index “cum LDL-C/age” to the development of coronary heart disease (CHD), myocardial infarction (MI), and a combined end point: MI, stroke, unstable angina in FH patients. Methods: 188 patients (mean age 49.2 years, males 45.7%) with FH were examined (Dutch Lipid Clinic Criteria). We had evaluated cumulative LDL-C and index “cum DL-C/age” along with other classical risk factors. Cum LDL-C was calculated as LDL-Cmax × (age at initiating of hypolipidemic therapy) + LDL-C at inclusion age at initiation/correction therapy). Cumulative LDL-C and “cum LDL-C/age” were calculated as the ratio cum LDL-C to age. The follow-up period was 5.4 (from 3 to 10) years. Results: The index “cum LDL-C/age” was higher in patients with CHD 58.7 ± 10.4 mmol/L/years vs. 40.1 ± 11.7 mmol/L/years in patients without CHD (p < 0.001). According to our data based on the results of the logistic regression analysis in patients with FH, cumulative LDL-C and the cumulative index “cum LDL–C/age” played a strong predictive role in the development of CHD in FH patients; it was greater than the role of TC and LDL-C concentrations. We present ROC curves for CHD, MI and combined end point in FH patients, and a prognostic scale for CHD development, which is based on classical cardiovascular risk factors. Conclusion: cumulative LDL-C level plays an important role in the development of CHD in FH patients. Full article

(This article belongs to the Special Issue Atherosclerosis: Technologies of Personalized Medicine)

► Show Figures

Figure 1

15 pages, 1767 KiB

Open AccessFeature PaperArticle

Associations of Antioxidant Enzymes with the Concentration of Fatty Acids in the Blood of Men with Coronary Artery Atherosclerosis

by Viktoriya S. Shramko, Eugeniia V. Striukova, Yana V. Polonskaya, Ekaterina M. Stakhneva, Marina V. Volkova, Alexey V. Kurguzov, Elena V. Kashtanova and Yuliya I. Ragino

J. Pers. Med. 2021, 11(12), 1281; https://doi.org/10.3390/jpm11121281 - 2 Dec 2021

Cited by 6 | Viewed by 1996

Abstract

Objective: To identify associations of fatty acids (FAs) with the antioxidant enzymes in the blood of men with coronary atherosclerosis and ischemic heart disease (IHD). Methods: The study included 80 patients: control group—20 men without IHD, the core group—60 men with IHD. The core group was divided into subgroups: subgroup A—with the presence of vulnerable atherosclerotic plaques, subgroup B—with the absence of vulnerable atherosclerotic plaques. We analyzed the levels of FAs, free radicals, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) in the blood. Results. Patients with IHD, compared with the control group: (1) had higher levels of SOD, CAT, myristic, palmitic, palmitoleic, and octadecenoic FAs; (2) had lower levels of GPx, α-linolenic, docosapentaenoic, docosahexaenoic, and arachidonic FAs. In subgroup A there were found: (1) negative associations of SOD—with linoleic, eicosatrienoic, arachidonic, eicosapentaenoic, docosapentaenoic and docosahexaenoic FAs, positive associations—with palmitic acid; (2) positive correlations of CAT level with palmitoleic and stearic acids; (3) negative associations between of GPx and palmitic, palmitoleic, stearic and octadecenoic FAs. Conclusions: Changes in the levels of antioxidant enzymes, and a disbalance of the FAs profile, probably indicate active oxidative processes in the body and may indicate the presence of atherosclerotic changes in the vessels. Full article

(This article belongs to the Special Issue Atherosclerosis: Technologies of Personalized Medicine)

► Show Figures

Figure 1

14 pages, 836 KiB

Open AccessArticle

Analysis of Rare Variants in Genes Related to Lipid Metabolism in Patients with Familial Hypercholesterolemia in Western Siberia (Russia)

by Elena Shakhtshneider, Dinara Ivanoshchuk, Olga Timoshchenko, Pavel Orlov, Sergey Semaev, Emil Valeev, Andrew Goonko, Nataliya Ladygina and Mikhail Voevoda

J. Pers. Med. 2021, 11(11), 1232; https://doi.org/10.3390/jpm11111232 - 19 Nov 2021

Cited by 8 | Viewed by 2409

Abstract

The aim of this work was to identify genetic variants potentially involved in familial hypercholesterolemia in 43 genes associated with lipid metabolism disorders. Targeted high-throughput sequencing of lipid metabolism genes was performed (80 subjects with a familial-hypercholesterolemia phenotype). For patients without functionally significant substitutions in the above genes, multiplex ligation-dependent probe amplification was conducted to determine bigger mutations (deletions and/or duplications) in the LDLR promoter and exons. A clinically significant variant in some gene associated with familial hypercholesterolemia was identified in 47.5% of the subjects. Clinically significant variants in the LDLR gene were identified in 19 probands (73.1% of all variants identified in probands); in three probands (11.5%), pathogenic variants were found in the APOB gene; and in four probands (15.4%), rare, clinically significant variants were identified in genes LPL, SREBF1, APOC3, and ABCG5. In 12 (85.7%) of 14 children of the probands, clinically significant variants were detectable in genes associated with familial hypercholesterolemia. The use of clinical criteria, targeted sequencing, and multiplex ligation-dependent probe amplification makes it possible to identify carriers of rare clinically significant variants in a wide range of lipid metabolism genes and to investigate their influence on phenotypic manifestations of familial hypercholesterolemia. Full article

(This article belongs to the Special Issue Atherosclerosis: Technologies of Personalized Medicine)

► Show Figures

Figure 1

13 pages, 1042 KiB

Open AccessFeature PaperArticle

Plateletworks^® as a Point-of-Care Test for ASA Non-Sensitivity

by Hamzah Khan, Shubha Jain, Reid C. Gallant, Muzammil H. Syed, Abdelrahman Zamzam, Mohammed Al-Omran, Margaret L. Rand, Heyu Ni, Rawand Abdin and Mohammad Qadura

J. Pers. Med. 2021, 11(8), 813; https://doi.org/10.3390/jpm11080813 - 20 Aug 2021

Cited by 3 | Viewed by 2375

Abstract

Aspirin (ASA) therapy is proven to be effective in preventing adverse cardiovascular events; however, up to 30% of patients are non-sensitive to their prescribed ASA dosage. In this pilot study, we demonstrated, for the first time, how ASA non-sensitivity can be diagnosed using Plateletworks^®, a point-of-care platelet function test. Patients prescribed 81 mg of ASA were recruited in a series of two successive phases—a discovery phase and a validation phase. In the discovery phase, a total of 60 patients were recruited to establish a cut-off point (COP) for ASA non-sensitivity using Plateletworks^®. Each sample was simultaneously cross-referenced with a light transmission aggregometer (LTA). Our findings demonstrated that >52% maximal platelet aggregation using Plateletworks^® had a sensitivity, specificity, and likelihood ratio of 80%, 70%, and 2.67, respectively, in predicting ASA non-sensitivity. This COP was validated in a secondary cohort of 40 patients prescribed 81 mg of ASA using Plateletworks^® and LTA. Our data demonstrated that our established COP had a 91% sensitivity and 69% specificity in identifying ASA non-sensitivity using Plateletworks^®. In summary, Plateletworks^® is a point-of-care platelet function test that can appropriately diagnose ASA non-sensitive patients with a sensitivity exceeding 80%. Full article

(This article belongs to the Special Issue Atherosclerosis: Technologies of Personalized Medicine)

► Show Figures

Figure 1

9 pages, 823 KiB

Open AccessArticle

Association of Matrix Metalloproteinases with Coronary Artery Calcification in Patients with CHD

by Yana V. Polonskaya, Elena V. Kashtanova, Ivan S. Murashov, Evgenia V. Striukova, Alexey V. Kurguzov, Ekaterina M. Stakhneva, Viktoria S. Shramko, Nikolay A. Maslatsov, Aleksandr M. Chernyavsky and Yulia I. Ragino

J. Pers. Med. 2021, 11(6), 506; https://doi.org/10.3390/jpm11060506 - 3 Jun 2021

Cited by 9 | Viewed by 2671

Abstract

This work is aimed at studying the relationship of matrix metalloproteinases with calcification of the coronary arteries. The study included 78 people with coronary heart disease (CHD) and 36 without CHD. Blood and samples of coronary arteries obtained as a result of endarterectomy were examined. Serum levels of metalloproteinases (MMP) MMP-1, MMP-2, MMP-3, MMP-7, MMP-9, MMP-10, MMP-12, and MMP-13 were determined by multiplex analysis. In blood vessel samples, MMP-1, MMP-3, MMP-7, and MMP-9 were determined by enzyme immunoassay; MMP-9 expression was evaluated by immunohistochemistry. Patients with CHD had higher serum levels of MMP-1, MMP-7, and MMP-12. Blood levels of MMP-1 and MMP-3 were associated with calcium levels, MMP-9 with osteoprotegerin and osteonectin, MMP-7 and MMP-10 with osteoprotegerin, MMP-12 with osteocalcin, and MMP-13 with osteopontin. Calcified plaques had higher levels of MMP-1 and MMP-9 compared to plaques without calcification. The relative risk of coronary arteries calcification was associated with MMP-9, which is confirmed by the results of immunohistochemistry. The results obtained indicate the participation of some MMPs, and especially MMP-9, in the calcification processes. The study can serve as a basis for the further study of the possibility of using MMP-1, MMP-7 and MMP-12 as potential biomarkers of CHD. Full article

(This article belongs to the Special Issue Atherosclerosis: Technologies of Personalized Medicine)

► Show Figures

Journal Menu

Journal Browser

Atherosclerosis: Technologies of Personalized Medicine

Share This Special Issue

Special Issue Editor

Special Issue Information

Keywords

Benefits of Publishing in a Special Issue

Published Papers (11 papers)

Editorial

Research

Further Information

Guidelines

MDPI Initiatives

Follow MDPI