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Cardiovascular Disease, Atherosclerosis and Familial Hypercholesterolemia: From Molecular Mechanisms Causing Pathogenicity till New Therapeutic Approaches

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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 (30 November 2020) | Viewed by 191564

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Special Issue Editor

Dr. César Martín

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Guest Editor

1. Department of Molecular Biophysics, Biofisika Institute, University of Basque Country and Consejo Superior de Investigaciones Científicas (UPV/EHU, CSIC), 48940 Leioa, Spain
2. Department of Biochemistry and Molecular Biology, Universidad del País Vasco UPV/EHU, 48080 Bilbao, Spain
Interests: familial hypercholesterolemia; low density lipoprotein receptor (LDLR); functional validation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular disease (CVD) remains the leading cause of death globally, taking an estimated 17.9 million lives each year. CVD is a general term that comprises many different types of conditions affecting the heart or blood vessels, which is generally associated with a build-up of fatty deposits inside the arteries (atherosclerosis) and an increased risk of blood clots, and can also be associated with damage to arteries in organs such as the brain, heart, kidneys, and eyes. The risk of CVD is affected by increased LDL cholesterol levels and is associated with several risk factors, including obesity, diabetes, smoking, hypertension, male sex, and age. Active engagement and more effective and appealing approaches to prevention, diagnosis, and treatment can be achieved by the medical and research community, which is important for furthering advances in clinical practice, training, and research in global health.

This Special Issue on “Cardiovascular Disease, Atherosclerosis and Familial Hypercholesterolemia: From Molecular Mechanisms Causing Pathogenicity to New Therapeutic Approaches” will collect reviews that address various aspects of the molecular aspects causing disease as well as research articles pointing out recent advances in the field.

Dr. César Martín
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

Familial hypercholesterolemia
Atherosclerosis
Cardiovascular disease
Type 2 diabetes
Epigenetic
Cholesterol
Dislipidemias
Therapies

Published Papers (5 papers)

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Research

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15 pages, 4309 KiB

Open AccessArticle

Effect of Fibroblast Growth Factor 21 on the Development of Atheromatous Plaque and Lipid Metabolic Profiles in an Atherosclerosis-Prone Mouse Model

by Hyo Jin Maeng, Gha Young Lee, Jae Hyun Bae and Soo Lim

Int. J. Mol. Sci. 2020, 21(18), 6836; https://doi.org/10.3390/ijms21186836 - 17 Sep 2020

Cited by 12 | Viewed by 2366

Abstract

Fibroblast growth factor 21 (FGF21) is a hormonal regulator of lipid and glucose metabolism. We aimed to investigate the effect of an FGF21 analogue (LY2405319) on the development of atherosclerosis and its associated parameters. ApoE^−/− mice were fed an atherogenic diet for 14 weeks and were randomly assigned to control (saline) or FGF21 (0.1 mg/kg) treatment group (n = 10/group) for 5 weeks. Plaque size in the aortic arch/valve areas and cardiovascular risk markers were evaluated in blood and tissues. The effects of FGF21 on various atherogenesis-related pathways were also assessed. Atherosclerotic plaque areas in the aortic arch/valve were significantly smaller in the FGF21 group than in controls after treatment. FGF21 significantly decreased body weight and glucose concentrations, and increased circulating adiponectin levels. FGF21 treatment alleviated insulin resistance and decreased circulating concentrations of triglycerides, which were significantly correlated with plaque size. FGF21 treatment reduced lipid droplets in the liver and decreased fat cell size and inflammatory cell infiltration in the abdominal visceral fat compared with the control group. The monocyte chemoattractant protein-1 levels were decreased and β-hydroxybutyrate levels were increased by FGF21 treatment. Uncoupling protein 1 expression in subcutaneous fat was greater and fat cell size in brown fat was smaller in the FGF21 group compared with controls. Administration of FGF21 showed anti-atherosclerotic effects in atherosclerosis-prone mice and exerted beneficial effects on critical atherosclerosis pathways. Improvements in inflammation and insulin resistance seem to be mechanisms involved in the mitigation of atherosclerosis by FGF21 therapy. Full article

(This article belongs to the Special Issue Cardiovascular Disease, Atherosclerosis and Familial Hypercholesterolemia: From Molecular Mechanisms Causing Pathogenicity till New Therapeutic Approaches)

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Review

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18 pages, 1055 KiB

Open AccessReview

Galectin-3 in Cardiovascular Diseases

by Valeria Blanda, Umberto Marcello Bracale, Maria Donata Di Taranto and Giuliana Fortunato

Int. J. Mol. Sci. 2020, 21(23), 9232; https://doi.org/10.3390/ijms21239232 - 03 Dec 2020

Cited by 84 | Viewed by 8312

Abstract

Galectin-3 (Gal-3) is a β-galactoside-binding protein belonging to the lectin family with pleiotropic regulatory activities and several physiological cellular functions, such as cellular growth, proliferation, apoptosis, differentiation, cellular adhesion, and tissue repair. Inflammation, tissue fibrosis and angiogenesis are the main processes in which Gal-3 is involved. It is implicated in the pathogenesis of several diseases, including organ fibrosis, chronic inflammation, cancer, atherosclerosis and other cardiovascular diseases (CVDs). This review aims to explore the connections of Gal-3 with cardiovascular diseases since they represent a major cause of morbidity and mortality. We herein discuss the evidence on the pro-inflammatory role of Gal-3 in the atherogenic process as well as the association with plaque features linked to lesion stability. We report the biological role and molecular mechanisms of Gal-3 in other CVDs, highlighting its involvement in the development of cardiac fibrosis and impaired myocardium remodelling, resulting in heart failure and atrial fibrillation. The role of Gal-3 as a prognostic marker of heart failure is described together with possible diagnostic applications to other CVDs. Finally, we report the tentative use of Gal-3 inhibition as a therapeutic approach to prevent cardiac inflammation and fibrosis. Full article

(This article belongs to the Special Issue Cardiovascular Disease, Atherosclerosis and Familial Hypercholesterolemia: From Molecular Mechanisms Causing Pathogenicity till New Therapeutic Approaches)

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34 pages, 3734 KiB

Open AccessReview

Pathophysiology of Type 2 Diabetes Mellitus

by Unai Galicia-Garcia, Asier Benito-Vicente, Shifa Jebari, Asier Larrea-Sebal, Haziq Siddiqi, Kepa B. Uribe, Helena Ostolaza and César Martín

Int. J. Mol. Sci. 2020, 21(17), 6275; https://doi.org/10.3390/ijms21176275 - 30 Aug 2020

Cited by 983 | Viewed by 160976

Abstract

Type 2 Diabetes Mellitus (T2DM), one of the most common metabolic disorders, is caused by a combination of two primary factors: defective insulin secretion by pancreatic β-cells and the inability of insulin-sensitive tissues to respond appropriately to insulin. Because insulin release and activity are essential processes for glucose homeostasis, the molecular mechanisms involved in the synthesis and release of insulin, as well as in its detection are tightly regulated. Defects in any of the mechanisms involved in these processes can lead to a metabolic imbalance responsible for the development of the disease. This review analyzes the key aspects of T2DM, as well as the molecular mechanisms and pathways implicated in insulin metabolism leading to T2DM and insulin resistance. For that purpose, we summarize the data gathered up until now, focusing especially on insulin synthesis, insulin release, insulin sensing and on the downstream effects on individual insulin-sensitive organs. The review also covers the pathological conditions perpetuating T2DM such as nutritional factors, physical activity, gut dysbiosis and metabolic memory. Additionally, because T2DM is associated with accelerated atherosclerosis development, we review here some of the molecular mechanisms that link T2DM and insulin resistance (IR) as well as cardiovascular risk as one of the most important complications in T2DM. Full article

(This article belongs to the Special Issue Cardiovascular Disease, Atherosclerosis and Familial Hypercholesterolemia: From Molecular Mechanisms Causing Pathogenicity till New Therapeutic Approaches)

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13 pages, 706 KiB

Open AccessReview

Noninvasive Testing for Diagnosis of Stable Coronary Artery Disease in the Elderly

by Sergey G. Kozlov, Olga V. Chernova, Elena V. Gerasimova, Ekaterina A. Ivanova and Alexander N. Orekhov

Int. J. Mol. Sci. 2020, 21(17), 6263; https://doi.org/10.3390/ijms21176263 - 29 Aug 2020

Cited by 2 | Viewed by 2969

Abstract

Efficient diagnostic approaches to detect coronary artery disease (CAD) in elderly patients are necessary to ensure optimal and timely treatment. The population of suspected CAD patients older than 70 years is especially vulnerable and constantly growing. Finding the optimal diagnostic approach is challenging due to certain features of this population, such as high prevalence of comorbidities, existing contraindications to exercise tests or cognitive decline, which hinders correct assessment of the patient’s situation. Moreover, some symptoms of CAD can have variable significance in the elderly compared to younger adult groups. In this review, we present current recommendations of the United States (US) and European cardiologists’ associations and discuss their applicability for diagnostics in the elderly population. Exercise electrocardiogram (ECG) and exercise stress echocardiography (SE) tests are not feasible for a substantial proportion of elderly patients. Coronary computed tomography angiography (CTA) appears to be an attractive alternative for such patients, but is not universally applicable; for instance, it is problematic in patients with significant calcification of the vessels. Moreover, more studies are needed to compare the results delivered by CTA to those of other diagnostic methods. Future efforts should be focused on comparative studies to better understand the limits and advantages of different diagnostic methods and their combinations. It is possible that some of the currently used diagnostic criteria could be improved to better accommodate the needs of the elderly population. Full article

(This article belongs to the Special Issue Cardiovascular Disease, Atherosclerosis and Familial Hypercholesterolemia: From Molecular Mechanisms Causing Pathogenicity till New Therapeutic Approaches)

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25 pages, 4336 KiB

Open AccessReview

Statin Treatment-Induced Development of Type 2 Diabetes: From Clinical Evidence to Mechanistic Insights

by Unai Galicia-Garcia, Shifa Jebari, Asier Larrea-Sebal, Kepa B. Uribe, Haziq Siddiqi, Helena Ostolaza, Asier Benito-Vicente and César Martín

Int. J. Mol. Sci. 2020, 21(13), 4725; https://doi.org/10.3390/ijms21134725 - 02 Jul 2020

Cited by 61 | Viewed by 15958

Abstract

Statins are the gold-standard treatment for the prevention of primary and secondary cardiovascular disease, which is the leading cause of mortality worldwide. Despite the safety and relative tolerability of statins, observational studies, clinical trials and meta-analyses indicate an increased risk of developing new-onset type 2 diabetes mellitus (T2DM) after long-term statin treatment. It has been shown that statins can impair insulin sensitivity and secretion by pancreatic β-cells and increase insulin resistance in peripheral tissues. The mechanisms involved in these processes include, among others, impaired Ca²⁺ signaling in pancreatic β-cells, down-regulation of GLUT-4 in adipocytes and compromised insulin signaling. In addition, it has also been described that statins’ impact on epigenetics may also contribute to statin-induced T2DM via differential expression of microRNAs. This review focuses on the evidence and mechanisms by which statin therapy is associated with the development of T2DM. This review describes the multifactorial combination of effects that most likely contributes to the diabetogenic effects of statins. Clinically, these findings should encourage clinicians to consider diabetes monitoring in patients receiving statin therapy in order to ensure early diagnosis and appropriate management. Full article

(This article belongs to the Special Issue Cardiovascular Disease, Atherosclerosis and Familial Hypercholesterolemia: From Molecular Mechanisms Causing Pathogenicity till New Therapeutic Approaches)

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