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Mechanisms of Cardiovascular Disease: Molecular Perspective 2.0

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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 April 2023) | Viewed by 15317

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Prof. Dr. Jan Pitha

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Guest Editor

Cardiology Department, Cardiovascular Centre, Institute for Clinical and Experimental Medicine, 140 21 Prague, Czech Republic
Interests: dyslipidemia; diabetes mellitus; vascular disease; atherosclerosis; inflammation; genetics; ischemic heart disease; heart failure; sex differences
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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 Pitha
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

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Published Papers (7 papers)

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Editorial

Jump to: Research, Review

4 pages, 187 KiB

Open AccessEditorial

From Cardiovascular Prevention and Differential Diagnosis to the Treatment of Myocardial Damage—Experimental and Human Perspectives

by Jan Pitha

Int. J. Mol. Sci. 2023, 24(23), 16997; https://doi.org/10.3390/ijms242316997 - 30 Nov 2023

Viewed by 822

Abstract

Cardiovascular diseases are characterized by many clinical, morphological, functional, and biochemical markers, including age, sex, genetic factors, plasma lipids, glycemia, and many other laboratory parameters [...] Full article

(This article belongs to the Special Issue Mechanisms of Cardiovascular Disease: Molecular Perspective 2.0)

Research

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8 pages, 752 KiB

Open AccessCommunication

Plasma Galectin-4 Levels Are Increased after Stroke in Mice and Humans

by Amra Jujic, João P. P. Vieira, Hana Matuskova, Peter M. Nilsson, Ulf Lindblad, Michael H. Olsen, João M. N. Duarte, Anja Meissner and Martin Magnusson

Int. J. Mol. Sci. 2023, 24(12), 10064; https://doi.org/10.3390/ijms241210064 - 13 Jun 2023

Cited by 3 | Viewed by 2034

Abstract

Epidemiological studies have associated plasma galectin-4 (Gal-4) levels with prevalent and incident diabetes, and with an increased risk of coronary artery disease. To date, data regarding possible associations between plasma Gal-4 and stroke are lacking. Using linear and logistic regression analyses, we tested Gal-4 association with prevalent stroke in a population-based cohort. Additionally, in mice fed a high-fat diet (HFD), we investigated whether plasma Gal-4 increases in response to ischemic stroke. Plasma Gal-4 was higher in subjects with prevalent ischemic stroke, and was associated with prevalent ischemic stroke (odds ratio 1.52; 95% confidence interval 1.01–2.30; p = 0.048) adjusted for age, sex, and covariates of cardiometabolic health. Plasma Gal-4 increased after experimental stroke in both controls and HFD-fed mice. HFD exposure was devoid of impact on Gal-4 levels. This study demonstrates higher plasma Gal-4 levels in both experimental stroke and in humans that experienced ischemic stroke. Full article

(This article belongs to the Special Issue Mechanisms of Cardiovascular Disease: Molecular Perspective 2.0)

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17 pages, 8650 KiB

Open AccessArticle

Exercise Training Attenuates Acute β-Adrenergic Receptor Activation-Induced Cardiac Inflammation via the Activation of AMP-Activated Protein Kinase

by Mi Zhang, Akehu Alemasi, Mingming Zhao, Wenli Xu, Youyi Zhang, Wei Gao, Haiyi Yu and Han Xiao

Int. J. Mol. Sci. 2023, 24(11), 9263; https://doi.org/10.3390/ijms24119263 - 25 May 2023

Cited by 2 | Viewed by 2081

Abstract

Exercise has proven cardiac benefits, but the underlying mechanisms of exercise that protect the heart from acute sympathetic stress injuries remain unknown. In this study, adult C57BL/6J mice and their AMP-activated protein kinase α2 knockout (AMPKα2^−/−) littermates were either subjected to 6 weeks of exercise training or housed under sedentary conditions and then treated with or without a single subcutaneous injection of the β-adrenergic receptor (β-AR) agonist isoprenaline (ISO). We investigated the differences in the protective effects of exercise training on ISO-induced cardiac inflammation in wild-type (WT) and AMPKα2^−/− mice using histology, enzyme-linked immunosorbent assay (ELISA) and Western blotting analyses. The results indicated that exercise training alleviated ISO-induced cardiac macrophage infiltration, chemokines and the expression of proinflammatory cytokines in wild-type mice. A mechanism study showed that exercise training attenuated the ISO-induced production of reactive oxygen species (ROS) and the activation of NLR Family, pyrin domain-containing 3 (NLRP3) inflammasomes. In cardiomyocytes, the ISO-induced effects on these processes were inhibited by AMP-activated protein kinase (AMPK) activator (metformin) pretreatment and reversed by the AMPK inhibitor (compound C). AMPKα2^−/− mice showed more extensive cardiac inflammation following ISO exposure than their wild-type littermates. These results indicated that exercise training could attenuate ISO-induced cardiac inflammation by inhibiting the ROS-NLRP3 inflammasome pathway in an AMPK-dependent manner. Our findings suggested the identification of a novel mechanism for the cardioprotective effects of exercise. Full article

(This article belongs to the Special Issue Mechanisms of Cardiovascular Disease: Molecular Perspective 2.0)

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25 pages, 5966 KiB

Open AccessArticle

Vitamin C Regulates the Profibrotic Activity of Fibroblasts in In Vitro Replica Settings of Myocardial Infarction

by Yichen Xu, Huabo Zheng, Pakhwan Nilcham, Octavian Bucur, Felix Vogt, Ioana Slabu, Elisa Anamaria Liehn and Mihaela Rusu

Int. J. Mol. Sci. 2023, 24(9), 8379; https://doi.org/10.3390/ijms24098379 - 6 May 2023

Cited by 4 | Viewed by 2366

Abstract

Extracellular collagen remodeling is one of the central mechanisms responsible for the structural and compositional coherence of myocardium in patients undergoing myocardial infarction (MI). Activated primary cardiac fibroblasts following myocardial infarction are extensively investigated to establish anti-fibrotic therapies to improve left ventricular remodeling. To systematically assess vitamin C functions as a potential modulator involved in collagen fibrillogenesis in an in vitro model mimicking heart tissue healing after MI. Mouse primary cardiac fibroblasts were isolated from wild-type C57BL/6 mice and cultured under normal and profibrotic (hypoxic + transforming growth factor beta 1) conditions on freshly prepared coatings mimicking extracellular matrix (ECM) remodeling during healing after an MI. At 10 μg/mL, vitamin C reprogramed the respiratory mitochondrial metabolism, which is effectively associated with a more increased accumulation of intracellular reactive oxygen species (iROS) than the number of those generated by mitochondrial reactive oxygen species (mROS). The mRNA/protein expression of subtypes I, III collagen, and fibroblasts differentiations markers were upregulated over time, particularly in the presence of vitamin C. The collagen substrate potentiated the modulator role of vitamin C in reinforcing the structure of types I and III collagen synthesis by reducing collagen V expression in a timely manner, which is important in the initiation of fibrillogenesis. Altogether, our study evidenced the synergistic function of vitamin C at an optimum dose on maintaining the equilibrium functionality of radical scavenger and gene transcription, which are important in the initial phases after healing after an MI, while modulating the synthesis of de novo collagen fibrils, which is important in the final stage of tissue healing. Full article

(This article belongs to the Special Issue Mechanisms of Cardiovascular Disease: Molecular Perspective 2.0)

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10 pages, 930 KiB

Open AccessArticle

Interest of Procalcitonin in ANCA Vasculitides for Differentiation between Flare and Infections

by Xavier Poirot-Seynaeve, Perrine Smets, Bruno Pereira, Louis Olagne, Julien Stievenart, Vincent Sapin, Olivier Aumaitre, Marc Andre and Ludovic Trefond

Int. J. Mol. Sci. 2023, 24(6), 5557; https://doi.org/10.3390/ijms24065557 - 14 Mar 2023

Cited by 1 | Viewed by 1692

Abstract

Procalcitonin (PCT) was established as a biomarker to discriminate bacterial infections from other proinflammatory conditions. Our objective was to determine whether PCT is effective in differentiating infection from antineutrophil-cytoplasmic-antibody (ANCA)-associated vasculitides (AAV) flare. In this retrospective, case-control study, PCT and other inflammatory biomarkers of patients with AAV relapse (relapsing group) were compared to infected AAV patients (infected group). In our population of 74 patients with AAV, PCT was significantly higher in the infected group than in the relapsing group (0.2 µg/L [0.08; 0.935] vs. 0.09 µg/L [0.05; 0.2], p < 0.001). Sensitivity and specificity were 53.4% and 73.6%, respectively, for an ideal threshold of 0.2 µg/L. C-reactive protein (CRP) was significantly higher in cases of infection than in relapse (64.7 mg/L [25; 131] vs. 31.5 mg/L, [10.6; 120], p = 0.001). Sensitivity and specificity for infections were 94.2% and 11.3%, respectively. Fibrinogen, white blood cell count, eosinophil count, and neutrophil count were not significantly different. In the multivariate analysis, the relative risk of infection was 2 [1.02; 4.5] (p = 0.04) for a PCT above 0.2 µg/L. In AAV, PCT may be useful for discriminating between infections and flare in patients suffering from AAVs. Full article

(This article belongs to the Special Issue Mechanisms of Cardiovascular Disease: Molecular Perspective 2.0)

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24 pages, 3967 KiB

Open AccessArticle

Endogenous Modulation of Extracellular Matrix Collagen during Scar Formation after Myocardial Infarction

by David Schumacher, Adelina Curaj, Mareike Staudt, Sakine Simsekyilmaz, Isabella Kanzler, Peter Boor, Barbara Mara Klinkhammer, Xiaofeng Li, Octavian Bucur, Adnan Kaabi, Yichen Xu, Huabo Zheng, Pakhwan Nilcham, Alexander Schuh, Mihaela Rusu and Elisa A. Liehn

Int. J. Mol. Sci. 2022, 23(23), 14571; https://doi.org/10.3390/ijms232314571 - 23 Nov 2022

Cited by 10 | Viewed by 2583

Abstract

Myocardial infarction is remains the leading cause of death in developed countries. Recent data show that the composition of the extracellular matrix might differ despite similar heart function and infarction sizes. Because collagen is the main component of the extracellular matrix, we hypothesized that changes in inflammatory cell recruitment influence the synthesis of different collagen subtypes in myofibroblasts, thus changing the composition of the scar. We found that neutrophils sustain the proliferation of fibroblasts, remodeling, differentiation, migration and inflammation, predominantly by IL-1 and PPARγ pathways (n = 3). They also significantly inhibit the mRNA expression of fibrillar collagen, maintaining a reduced stiffness in isolated myofibroblasts (n = 4–5). Reducing the neutrophil infiltration in CCR1^−/− resulted in increased mRNA expression of collagen 11, moderate expression of collagen 19 and low expression of collagen 13 and 26 in the scar 4 weeks post infarction compared with other groups (n = 3). Mononuclear cells increased the synthesis of all collagen subtypes and upregulated the NF-kB, angiotensin II and PPARδ pathways (n = 3). They increased the synthesis of collagen subtypes 1, 3, 5, 16 and 23 but reduced the expression of collagens 5 and 16 (n = 3). CCR2^−/− scar tissue showed higher levels of collagen 13 (n = 3), in association with a significant reduction in stiffness (n = 4–5). Upregulation of the inflammation-related genes in myofibroblasts mostly modulated the fibrillar collagen subtypes, with less effect on the FACIT, network-forming and globular subtypes (n = 3). The upregulation of proliferation and differentiation genes in myofibroblasts seemed to be associated only with the fibrillar collagen subtype, whereas angiogenesis-related genes are associated with fibrillar, network-forming and multiplexin subtypes. In conclusion, although we intend for our findings to deepen the understanding of the mechanism of healing after myocardial infarction and scar formation, the process of collagen synthesis is highly complex, and further intensive investigation is needed to put together all the missing puzzle pieces in this still incipient knowledge process. Full article

(This article belongs to the Special Issue Mechanisms of Cardiovascular Disease: Molecular Perspective 2.0)

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Review

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13 pages, 340 KiB

Open AccessReview

Molecular Mechanisms of Takotsubo Syndrome

by Liam S. Couch, Keith Channon and Thomas Thum

Int. J. Mol. Sci. 2022, 23(20), 12262; https://doi.org/10.3390/ijms232012262 - 14 Oct 2022

Cited by 10 | Viewed by 2630

Abstract

Takotsubo syndrome (TTS) is a severe but reversible acute heart failure syndrome that occurs following high catecholaminergic stress. TTS patients are similar to those with acute coronary syndrome, with chest pain, dyspnoea and ST segment changes on electrocardiogram, but are characterised by apical akinesia of the left ventricle, with basal hyperkinesia in the absence of culprit coronary artery stenosis. The pathophysiology of TTS is not completely understood and there is a paucity of evidence to guide treatment. The mechanisms of TTS are thought to involve catecholaminergic myocardial stunning, microvascular dysfunction, increased inflammation and changes in cardiomyocyte metabolism. Here, we summarise the available literature to focus on the molecular basis for the pathophysiology of TTS to advance the understanding of the condition. Full article

(This article belongs to the Special Issue Mechanisms of Cardiovascular Disease: Molecular Perspective 2.0)

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