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Mechanisms of Cardiovascular Disease: Molecular Perspective

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 41145

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Special Issue Editor

Prof. Dr. Jan Pitha

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Guest Editor

Clinic of Cardiology, Laboratory for Atherosclerosis Research, Centre for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic
Interests: dyslipidemia; diabetes mellitus; vascular disease; atherosclerosis; inflammation; genetics; ischemic heart disease; heart failure sex differences
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We hope that you, your families and friends are doing well in these days. As the guest editors, we would like to invite you to contribute a research paper or review article for peer-review and potentially publication in Special Issue of IJMS entitled “Mechanisms of Cardiovascular Disease: Molecular Perspective”. We would like to encourage you to submit articles focused on experimental research investigating (sub)molecular mechanisms of the structural and functional disorders of the heart and blood vessels. Priority will be given to articles focused on metabolic, hormonal, inflammatory, and (epi)genetic processes involved in cardiovascular disease. As indicated, articles should be from the fields of experimental and/or molecular research. Therefore, clinical studies such as case reports, clinical surveys and epidemiological studies are not suitable.

Prof. Dr. Jan Piťha
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

heart failure
ischemic heart disease
vascular disease
diabetes mellitus
inflammation
dyslipidemia
gene regulation

Published Papers (11 papers)

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Research

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29 pages, 15657 KiB

Open AccessArticle

Vascular Remodeling of Clinically Used Patches and Decellularized Pericardial Matrices Recellularized with Autologous or Allogeneic Cells in a Porcine Carotid Artery Model

by Jaroslav Chlupac, Roman Matejka, Miroslav Konarik, Robert Novotny, Zuzana Simunkova, Iveta Mrazova, Ondrej Fabian, Milan Zapletal, Zdenek Pulda, Jan Falk Lipensky, Jana Stepanovska, Karel Hanzalek, Antonin Broz, Tomas Novak, Alena Lodererova, Ludek Voska, Theodor Adla, Jiri Fronek, Miroslav Rozkot, Serhiy Forostyak, Peter Kneppo, Lucie Bacakova and Jan Pirk Show full author list Hide full author list

Int. J. Mol. Sci. 2022, 23(6), 3310; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23063310 - 18 Mar 2022

Cited by 7 | Viewed by 4012

Abstract

Background: Cardiovascular surgery is confronted by a lack of suitable materials for patch repair. Acellular animal tissues serve as an abundant source of promising biomaterials. The aim of our study was to explore the bio-integration of decellularized or recellularized pericardial matrices in vivo. Methods: Porcine (allograft) and ovine (heterograft, xenograft) pericardia were decellularized using 1% sodium dodecyl sulfate ((1) Allo-decel and (2) Xeno-decel). We used two cell types for pressure-stimulated recellularization in a bioreactor: autologous adipose tissue-derived stromal cells (ASCs) isolated from subcutaneous fat of pigs ((3) Allo-ASC and (4) Xeno-ASC) and allogeneic Wharton’s jelly mesenchymal stem cells (WJCs) ((5) Allo-WJC and (6) Xeno-WJC). These six experimental patches were implanted in porcine carotid arteries for one month. For comparison, we also implanted six types of control patches, namely, arterial or venous autografts, expanded polytetrafluoroethylene (ePTFE Propaten^® Gore^®), polyethylene terephthalate (PET Vascutek^®), chemically stabilized bovine pericardium (XenoSure^®), and detoxified porcine pericardium (BioIntegral^® NoReact^®). The grafts were evaluated through the use of flowmetry, angiography, and histological examination. Results: All grafts were well-integrated and patent with no signs of thrombosis, stenosis, or aneurysm. A histological analysis revealed that the arterial autograft resembled a native artery. All other control and experimental patches developed neo-adventitial inflammation (NAI) and neo-intimal hyperplasia (NIH), and the endothelial lining was present. NAI and NIH were most prominent on XenoSure^® and Xeno-decel and least prominent on NoReact^®. In xenografts, the degree of NIH developed in the following order: Xeno-decel > Xeno-ASC > Xeno-WJC. NAI and patch resorption increased in Allo-ASC and Xeno-ASC and decreased in Allo-WJC and Xeno-WJC. Conclusions: In our setting, pre-implant seeding with ASC or WJC had a modest impact on vascular patch remodeling. However, ASC increased the neo-adventitial inflammatory reaction and patch resorption, suggesting accelerated remodeling. WJC mitigated this response, as well as neo-intimal hyperplasia on xenografts, suggesting immunomodulatory properties. Full article

(This article belongs to the Special Issue Mechanisms of Cardiovascular Disease: Molecular Perspective)

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16 pages, 2168 KiB

Open AccessArticle

Cardiovascular, Metabolic and Inflammatory Changes after Ovariectomy and Estradiol Substitution in Hereditary Hypertriglyceridemic Rats

by Jan Pitha, Martina Huttl, Hana Malinska, Denisa Miklankova, Hana Bartuskova, Tomas Hlinka and Irena Markova

Int. J. Mol. Sci. 2022, 23(5), 2825; https://doi.org/10.3390/ijms23052825 - 04 Mar 2022

Cited by 2 | Viewed by 1875

Abstract

Background: If menopause is really independent risk factor for cardiovascular disease is still under debate. We studied if ovariectomy in the model of insulin resistance causes cardiovascular changes, to what extent are these changes reversible by estradiol substitution and if they are accompanied by changes in other organs and tissues. Methods: Hereditary hypertriglyceridemic female rats were divided into three groups: ovariectomized at 8th week (n = 6), ovariectomized with 17-β estradiol substitution (n = 6), and the sham group (n = 5). The strain of abdominal aorta measured by ultrasound, expression of vascular genes, weight and content of myocardium and also non-cardiac parameters were analyzed. Results: After ovariectomy, the strain of abdominal aorta, expression of nitric oxide synthase in abdominal aorta, relative weight of myocardium and of the left ventricle and circulating interleukin-6 decreased; these changes were reversed by estradiol substitution. Interestingly, the content of triglycerides in myocardium did not change after ovariectomy, but significantly increased after estradiol substitution while adiposity index did not change after ovariectomy, but significantly decreased after estradiol substitution. Conclusion: Vascular and cardiac parameters under study differed in their response to ovariectomy and estradiol substitution. This indicates different effects of ovariectomy and estradiol on different cardiovascular but also extracardiac structures. Full article

(This article belongs to the Special Issue Mechanisms of Cardiovascular Disease: Molecular Perspective)

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10 pages, 6501 KiB

Open AccessArticle

Cell Viability Assessment Using Fluorescence Vital Dyes and Confocal Microscopy in Evaluating Freezing and Thawing Protocols Used in Cryopreservation of Allogeneic Venous Grafts

by Pavel Měřička, Libor Janoušek, Aleš Benda, Radka Lainková, Ján Sabó, Markéta Dalecká, Petra Prokšová, Myroslav Salmay, Rudolf Špunda, Ondřej Pecha, Miroslava Jandová, Jiří Gregor, Lubomír Štěrba, Miroslav Špaček and Jaroslav Lindner

Int. J. Mol. Sci. 2021, 22(19), 10653; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221910653 - 30 Sep 2021

Cited by 2 | Viewed by 1786

Abstract

The authors present their contribution to the improvement of methods suitable for the detection of the freezing and thawing damage of cells of cryopreserved venous grafts used for lower limb revascularization procedures. They studied the post-thaw viability of cells of the wall of cryopreserved venous grafts (CVG) immediately after thawing and after 24 and 48 h culture at +37 °C in two groups of six CVG selected randomly for slow thawing in the refrigerator and rapid thawing in a water bath at +37 °C. The grafts were collected from multi-organ and tissue brain-dead donors, cryopreserved, and stored in a liquid nitrogen vapor phase for five years. The viability was assessed from tissue slices obtained by perpendicular and longitudinal cuts of the thawed graft samples using in situ staining with fluorescence vital dyes. The mean and median immediate post-thaw viability values above 70% were found in using both thawing protocols and both types of cutting. The statistically significant decline in viability after the 48-h culture was observed only when using the slow thawing protocol and perpendicular cutting. The possible explanation might be the “solution effect damage” during slow thawing, which caused a gentle reduction in the graft cellularity. The possible influence of this phenomenon on the immunogenicity of CVG should be the subject of further investigations. Full article

(This article belongs to the Special Issue Mechanisms of Cardiovascular Disease: Molecular Perspective)

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13 pages, 2355 KiB

Open AccessArticle

Nitro-Oleic Acid (NO₂-OA) Improves Systolic Function in Dilated Cardiomyopathy by Attenuating Myocardial Fibrosis

by Simon Braumann, Wibke Schumacher, Nam Gyu Im, Felix Sebastian Nettersheim, Dennis Mehrkens, Senai Bokredenghel, Alexander Hof, Richard Julius Nies, Christoph Adler, Holger Winkels, Ralph Knöll, Bruce A. Freeman, Volker Rudolph, Anna Klinke, Matti Adam, Stephan Baldus, Martin Mollenhauer and Simon Geißen

Int. J. Mol. Sci. 2021, 22(16), 9052; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22169052 - 22 Aug 2021

Cited by 6 | Viewed by 2811

Abstract

Nitro-oleic acid (NO₂-OA), a nitric oxide (NO)- and nitrite (NO₂⁻)-derived electrophilic fatty acid metabolite, displays anti-inflammatory and anti-fibrotic signaling actions and therapeutic benefit in murine models of ischemia-reperfusion, atrial fibrillation, and pulmonary hypertension. Muscle LIM protein-deficient mice (Mlp^−/−) develop dilated cardiomyopathy (DCM), characterized by impaired left ventricular function and increased ventricular fibrosis at the age of 8 weeks. This study investigated the effects of NO₂-OA on cardiac function in Mlp^−/− mice both in vivo and in vitro. Mlp^−/− mice were treated with NO₂-OA or vehicle for 4 weeks via subcutaneous osmotic minipumps. Wildtype (WT) littermates treated with vehicle served as controls. Mlp^−/− mice exhibited enhanced TGFβ signalling, fibrosis and severely reduced left ventricular systolic function. NO₂-OA treatment attenuated interstitial myocardial fibrosis and substantially improved left ventricular systolic function in Mlp^−/− mice. In vitro studies of TGFβ-stimulated primary cardiac fibroblasts further revealed that the anti-fibrotic effects of NO₂-OA rely on its capability to attenuate fibroblast to myofibroblast transdifferentiation by inhibiting phosphorylation of TGFβ downstream targets. In conclusion, we demonstrate a substantial therapeutic benefit of NO₂-OA in a murine model of DCM, mediated by interfering with endogenously activated TGFβ signaling. Full article

(This article belongs to the Special Issue Mechanisms of Cardiovascular Disease: Molecular Perspective)

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22 pages, 5953 KiB

Open AccessArticle

Kidney Response to Chemotherapy-Induced Heart Failure: mRNA Analysis in Normotensive and Ren-2 Transgenic Hypertensive Rats

by Šárka Jíchová, Olga Gawryś, Elżbieta Kompanowska-Jezierska, Janusz Sadowski, Vojtěch Melenovský, Lenka Hošková, Luděk Červenka, Petr Kala, Josef Veselka and Věra Čertíková Chábová

Int. J. Mol. Sci. 2021, 22(16), 8475; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22168475 - 06 Aug 2021

Viewed by 1526

Abstract

The aim of the present study was to perform kidney messenger ribonucleic acid (mRNA) analysis in normotensive, Hannover Sprague–Dawley (HanSD) rats and hypertensive, Ren-2 renin transgenic rats (TGR) after doxorubicin-induced heart failure (HF) with specific focus on genes that are implicated in the pathophysiology of HF-associated cardiorenal syndrome. We found that in both strains renin and angiotensin-converting enzyme mRNA expressions were upregulated indicating that the vasoconstrictor axis of the renin–angiotensin system was activated. We found that pre-proendothelin-1, endothelin-converting enzyme type 1 and endothelin type A receptor mRNA expressions were upregulated in HanSD rats, but not in TGR, suggesting the activation of endothelin system in HanSD rats, but not in TGR. We found that mRNA expression of cytochrome P-450 subfamily 2C23 was downregulated in TGR and not in HanSD rats, suggesting the deficiency in the intrarenal cytochrome P450-dependent pathway of arachidonic acid metabolism in TGR. These results should be the basis for future studies evaluating the pathophysiology of cardiorenal syndrome secondary to chemotherapy-induced HF in order to potentially develop new therapeutic approaches. Full article

(This article belongs to the Special Issue Mechanisms of Cardiovascular Disease: Molecular Perspective)

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17 pages, 2812 KiB

Open AccessArticle

Metformin Affects Cardiac Arachidonic Acid Metabolism and Cardiac Lipid Metabolite Storage in a Prediabetic Rat Model

by Denisa Miklankova, Irena Markova, Martina Hüttl, Iveta Zapletalova, Martin Poruba and Hana Malinska

Int. J. Mol. Sci. 2021, 22(14), 7680; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22147680 - 19 Jul 2021

Cited by 9 | Viewed by 2303

Abstract

Metformin can reduce cardiovascular risk independent of glycemic control. The mechanisms behind its non-glycemic benefits, which include decreased energy intake, lower blood pressure and improved lipid and fatty acid metabolism, are not fully understood. In our study, metformin treatment reduced myocardial accumulation of neutral lipids—triglycerides, cholesteryl esters and the lipotoxic intermediates—diacylglycerols and lysophosphatidylcholines in a prediabetic rat model (p < 0.001). We observed an association between decreased gene expression and SCD-1 activity (p < 0.05). In addition, metformin markedly improved phospholipid fatty acid composition in the myocardium, represented by decreased SFA profiles and increased n3-PUFA profiles. Known for its cardioprotective and anti-inflammatory properties, metformin also had positive effects on arachidonic acid metabolism and CYP-derived arachidonic acid metabolites. We also found an association between increased gene expression of the cardiac isoform CYP2c with increased 14,15-EET (p < 0.05) and markedly reduced 20-HETE (p < 0.001) in the myocardium. Based on these results, we conclude that metformin treatment reduces the lipogenic enzyme SCD-1 and the accumulation of the lipotoxic intermediates diacylglycerols and lysophosphatidylcholine. Increased CYP2c gene expression and beneficial effects on CYP-derived arachidonic acid metabolites in the myocardium can also be involved in cardioprotective effect of metformin. Full article

(This article belongs to the Special Issue Mechanisms of Cardiovascular Disease: Molecular Perspective)

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14 pages, 1607 KiB

Open AccessArticle

An Integrative Study of Aortic mRNA/miRNA Longitudinal Changes in Long-Term LVAD Support

by Dana Dlouha, Peter Ivak, Ivan Netuka, Sarka Benesova, Zuzana Tucanova and Jaroslav A. Hubacek

Int. J. Mol. Sci. 2021, 22(14), 7414; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22147414 - 10 Jul 2021

Cited by 2 | Viewed by 1755

Abstract

Studying the long-term impact of continuous-flow left ventricular assist device (CF-LVAD) offers an opportunity for a complex understanding of the pathophysiology of vascular changes in aortic tissue in response to a nonphysiological blood flow pattern. Our study aimed to analyze aortic mRNA/miRNA expression changes in response to long-term LVAD support. Paired aortic samples obtained at the time of LVAD implantation and at the time of heart transplantation were examined for mRNA/miRNA profiling. The number of differentially expressed genes (Pcorr < 0.05) shared between samples before and after LVAD support was 277. The whole miRNome profile revealed 69 differentially expressed miRNAs (Pcorr < 0.05). Gene ontology (GO) analysis identified that LVAD predominantly influenced genes involved in the extracellular matrix and collagen fibril organization. Integrated mRNA/miRNA analysis revealed that potential targets of miRNAs dysregulated in explanted samples are mainly involved in GO biological process terms related to dendritic spine organization, neuron projection organization, and cell junction assembly and organization. We found differentially expressed genes participating in vascular tissue engineering as a consequence of LVAD duration. Changes in aortic miRNA levels demonstrated an effect on molecular processes involved in angiogenesis. Full article

(This article belongs to the Special Issue Mechanisms of Cardiovascular Disease: Molecular Perspective)

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10 pages, 1272 KiB

Open AccessArticle

Different Expression of Mitochondrial and Endoplasmic Reticulum Stress Genes in Epicardial Adipose Tissue Depends on Coronary Atherosclerosis

by Helena Kratochvílová, Miloš Mráz, Barbora J. Kasperová, Daniel Hlaváček, Jakub Mahrík, Ivana Laňková, Anna Cinkajzlová, Zdeněk Matloch, Zdeňka Lacinová, Jaroslava Trnovská, Peter Ivák, Peter Novodvorský, Ivan Netuka and Martin Haluzík

Int. J. Mol. Sci. 2021, 22(9), 4538; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094538 - 26 Apr 2021

Cited by 5 | Viewed by 1939

Abstract

The aim of our study was to analyze mitochondrial and endoplasmic reticulum (ER) gene expression profiles in subcutaneous (SAT) and epicardial (EAT) adipose tissue, skeletal muscle, and myocardium in patients with and without CAD undergoing elective cardiac surgery. Thirty-eight patients, 27 with (CAD group) and 11 without CAD (noCAD group), undergoing coronary artery bypass grafting and/or valvular surgery were included in the study. EAT, SAT, intercostal skeletal muscle, and right atrium tissue and blood samples were collected at the start and end of surgery; mRNA expression of selected mitochondrial and ER stress genes was assessed using qRT-PCR. The presence of CAD was associated with decreased mRNA expression of most of the investigated mitochondrial respiratory chain genes in EAT, while no such changes were seen in SAT or other tissues. In contrast, the expression of ER stress genes did not differ between the CAD and noCAD groups in almost any tissue. Cardiac surgery further augmented mitochondrial dysfunction in EAT. In our study, CAD was associated with decreased expression of mitochondrial, but not endoplasmic reticulum stress genes in EAT. These changes may contribute to the acceleration of coronary atherosclerosis. Full article

(This article belongs to the Special Issue Mechanisms of Cardiovascular Disease: Molecular Perspective)

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Review

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44 pages, 1901 KiB

Open AccessReview

An Overview of the Cardiorenal Protective Mechanisms of SGLT2 Inhibitors

by Teresa Salvatore, Raffaele Galiero, Alfredo Caturano, Luca Rinaldi, Anna Di Martino, Gaetana Albanese, Jessica Di Salvo, Raffaella Epifani, Raffaele Marfella, Giovanni Docimo, Miriam Lettieri, Celestino Sardu and Ferdinando Carlo Sasso

Int. J. Mol. Sci. 2022, 23(7), 3651; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23073651 - 26 Mar 2022

Cited by 71 | Viewed by 14949

Abstract

Sodium-glucose co-transporter 2 (SGLT2) inhibitors block glucose reabsorption in the renal proximal tubule, an insulin-independent mechanism that plays a critical role in glycemic regulation in diabetes. In addition to their glucose-lowering effects, SGLT2 inhibitors prevent both renal damage and the onset of chronic kidney disease and cardiovascular events, in particular heart failure with both reduced and preserved ejection fraction. These unexpected benefits prompted changes in treatment guidelines and scientific interest in the underlying mechanisms. Aside from the target effects of SGLT2 inhibition, a wide spectrum of beneficial actions is described for the kidney and the heart, even though the cardiac tissue does not express SGLT2 channels. Correction of cardiorenal risk factors, metabolic adjustments ameliorating myocardial substrate utilization, and optimization of ventricular loading conditions through effects on diuresis, natriuresis, and vascular function appear to be the main underlying mechanisms for the observed cardiorenal protection. Additional clinical advantages associated with using SGLT2 inhibitors are antifibrotic effects due to correction of inflammation and oxidative stress, modulation of mitochondrial function, and autophagy. Much research is required to understand the numerous and complex pathways involved in SGLT2 inhibition. This review summarizes the current known mechanisms of SGLT2-mediated cardiorenal protection. Full article

(This article belongs to the Special Issue Mechanisms of Cardiovascular Disease: Molecular Perspective)

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20 pages, 2441 KiB

Open AccessReview

Omega-3 Polyunsaturated Fatty Acids—Vascular and Cardiac Effects on the Cellular and Molecular Level (Narrative Review)

by Ines Drenjančević and Jan Pitha

Int. J. Mol. Sci. 2022, 23(4), 2104; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23042104 - 14 Feb 2022

Cited by 15 | Viewed by 3556

Abstract

In the prevention and treatment of cardiovascular disease, in addition to the already proven effective treatment of dyslipidemia, hypertension and diabetes mellitus, omega-3 polyunsaturated fatty acids (n-3 PUFAs) are considered as substances with additive effects on cardiovascular health. N-3 PUFAs combine their indirect effects on metabolic, inflammatory and thrombogenic parameters with direct effects on the cellular level. Eicosapentaenoic acid (EPA) seems to be more efficient than docosahexaenoic acid (DHA) in the favorable mitigation of atherothrombosis due to its specific molecular properties. The inferred mechanism is a more favorable effect on the cell membrane. In addition, the anti-fibrotic effects of n-3 PUFA were described, with potential impacts on heart failure with a preserved ejection fraction. Furthermore, n-3 PUFA can modify ion channels, with a favorable impact on arrhythmias. However, despite recent evidence in the prevention of cardiovascular disease by a relatively high dose of icosapent ethyl (EPA derivative), there is still a paucity of data describing the exact mechanisms of n-3 PUFAs, including the role of their particular metabolites. The purpose of this review is to discuss the effects of n-3 PUFAs at several levels of the cardiovascular system, including controversies. Full article

(This article belongs to the Special Issue Mechanisms of Cardiovascular Disease: Molecular Perspective)

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19 pages, 1573 KiB

Open AccessReview

Nature versus Number: Monocytes in Cardiovascular Disease

by Helen Williams, Corinne D. Mack, Stephen C. H. Li, John P. Fletcher and Heather J. Medbury

Int. J. Mol. Sci. 2021, 22(17), 9119; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22179119 - 24 Aug 2021

Cited by 19 | Viewed by 2902

Abstract

Monocytes play a key role in cardiovascular disease (CVD) as their influx into the vessel wall is necessary for the development of an atherosclerotic plaque. Monocytes are, however, heterogeneous differentiating from classical monocytes through the intermediate subset to the nonclassical subset. While it is recognized that the percentage of intermediate and nonclassical monocytes are higher in individuals with CVD, accompanying changes in inflammatory markers suggest a functional impact on disease development that goes beyond the increased proportion of these ‘inflammatory’ monocyte subsets. Furthermore, emerging evidence indicates that changes in monocyte proportion and function arise in dyslipidemia, with lipid lowering medication having some effect on reversing these changes. This review explores the nature and number of monocyte subsets in CVD addressing what they are, when they arise, the effect of lipid lowering treatment, and the possible implications for plaque development. Understanding these associations will deepen our understanding of the clinical significance of monocytes in CVD. Full article

(This article belongs to the Special Issue Mechanisms of Cardiovascular Disease: Molecular Perspective)

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