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A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Cardiovascular System".

Deadline for manuscript submissions: closed (15 October 2023) | Viewed by 25272

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Special Issue Editors

Dr. Ying Wang

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Guest Editor

Department of Pharmacology, School of Medicine, University of California, One Shield Avenue, Davis, CA 95616, USA
Interests: cardiac biology and pathology; spatiotemporal regulation of cardiac adrenergic signaling; G-protein coupled receptors; PKA; calcium regulation; heart failure; inflammation; myocardial infarction; diabetic cardiomyopathy

Dr. Haocheng Lu

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Guest Editor

Department of Pharmacology, Southern University of Science and Technology, Shenzhen 518055, Guangdong, China
Interests: cardiovascular diseases; atherosclerosis; aortic aneurysm; angiogenesis; smooth muscle cell; macrophage; endothelial cell; inflammation; apoptosis; autophagy; diabetes; obesity

Prof. Dr. Yi Zhun Zhu

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Guest Editor

1. School of Pharmacy and State Key Lab. of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macao 999078, China
2. Shanghai Key Laboratory of Bioactive Small Molecules, Department of Pharmacology, School of Pharmacy, Fudan University, Shanghai 201203, China
Interests: inflammation; immune response; hydrogen sulfide; molecular mechanisms; drug discovery, natural product research, pharmacology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular diseases (CVDs) are the leading cause of global mortality and present huge unmet medical demands worldwide. Here, we aim to establish a Special Issue to provide cutting-edge insights into cardiovascular system biology and CVDs pathogenesis by publishing high-quality research articles, reviews, commentary, editorials, and short communications related to various aspects of cardiovascular biology, physiology, and pathology. The topics include but are not limited to the following:

GPCR signaling transduction and regulation in cardiovascular systems;
Calcium Regulation;
Cardiovascular remodeling: inflammation and fibrosis;
Cell-cell communication in cardiovascular systems;
Heart failure;
Atherosclerosis;
Hypertension.

This Special Issue aims to advance the current knowledge of all genetic, epigenetic, molecular, and signal regulation on cardiovascular biology, physiology, and pathological remodeling and highlights the potential therapeutic targets and strategies for managing CVDs. Studies in all the above-related fields are invited to contribute to this Special Issue. Particularly, we encourage the submission of studies that combines the integrative approaches of bioinformatics, transgenic animal model, and molecular biology.

We look forward to your contributions.

Dr. Ying Wang
Dr. Haocheng Lu
Prof. Dr. Yi Zhun Zhu
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. Cells is an international peer-reviewed open access semimonthly 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

GPCR signaling regulation in cardiovascular systems
calcium regulation
inflammation
aging
epigenetic regulation in cardiovascular physiology and pathology
genetics and gene therapy
cell–cell communication
heart failure
atherosclerosis
hypertension

Published Papers (9 papers)

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Research

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15 pages, 4428 KiB

Open AccessArticle

Effects of Acute and Chronic Gabapentin Treatment on Cardiovascular Function of Rats

by Ved Vasishtha Pendyala, Sarah Pribil, Victoria Schaal, Kanika Sharma, Sankarasubramanian Jagadesan, Li Yu, Vikas Kumar, Chittibabu Guda and Lie Gao

Cells 2023, 12(23), 2705; https://doi.org/10.3390/cells12232705 - 25 Nov 2023

Viewed by 2472

Abstract

Gabapentin (GBP), a GABA analogue, is primarily used as an anticonvulsant for the treatment of partial seizures and neuropathic pain. Whereas a majority of the side effects are associated with the nervous system, emerging evidence suggests there is a high risk of heart diseases in patients taking GBP. In the present study, we first used a preclinical model of rats to investigate, firstly, the acute cardiovascular responses to GBP (bolus i.v. injection, 50 mg/kg) and secondly the effects of chronic GBP treatment (i.p. 100 mg/kg/day × 7 days) on cardiovascular function and the myocardial proteome. Under isoflurane anesthesia, rat blood pressure (BP), heart rate (HR), and left ventricular (LV) hemodynamics were measured using Millar pressure transducers. The LV myocardium and brain cortex were analyzed by proteomics, bioinformatics, and western blot to explore the molecular mechanisms underlying GBP-induced cardiac dysfunction. In the first experiment, we found that i.v. GBP significantly decreased BP, HR, maximal LV pressure, and maximal and minimal dP/dt, whereas it increased IRP-AdP/dt, Tau, systolic, diastolic, and cycle durations (* p < 0.05 and ** p < 0.01 vs. baseline; n = 4). In the second experiment, we found that chronic GBP treatment resulted in hypotension, bradycardia, and LV systolic dysfunction, with no change in plasma norepinephrine. In the myocardium, we identified 109 differentially expressed proteins involved in calcium pathways, cholesterol metabolism, and galactose metabolism. Notably, we found that calmodulin, a key protein of intracellular calcium signaling, was significantly upregulated by GBP in the heart but not in the brain. In summary, we found that acute and chronic GBP treatments suppressed cardiovascular function in rats, which is attributed to abnormal calcium signaling in cardiomyocytes. These data reveal a novel side effect of GBP independent of the nervous system, providing important translational evidence to suggest that GBP can evoke adverse cardiovascular events by depression of myocardial function. Full article

(This article belongs to the Special Issue Research Advances Related to Cardiovascular System)

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20 pages, 4444 KiB

Open AccessArticle

Oral Administration of Rhamnan Sulfate from Monostroma nitidum Suppresses Atherosclerosis in ApoE-Deficient Mice Fed a High-Fat Diet

by Masahiro Terasawa, Liqing Zang, Keiichi Hiramoto, Yasuhito Shimada, Mari Mitsunaka, Ryota Uchida, Kaoru Nishiura, Koichi Matsuda, Norihiro Nishimura and Koji Suzuki

Cells 2023, 12(22), 2666; https://doi.org/10.3390/cells12222666 - 20 Nov 2023

Cited by 1 | Viewed by 1523

Abstract

Oral administration of rhamnan sulfate (RS), derived from the seaweed Monostroma nitidum, markedly suppresses inflammatory damage in the vascular endothelium and organs of lipopolysaccharide-treated mice. This study aimed to analyze whether orally administered RS inhibits the development of atherosclerosis, a chronic inflammation of the arteries. ApoE-deficient female mice were fed a normal or high-fat diet (HFD) with or without RS for 12 weeks. Immunohistochemical and mRNA analyses of atherosclerosis-related genes were performed. The effect of RS on the migration of RAW264.7 cells was also examined in vitro. RS administration suppressed the increase in blood total cholesterol and triglyceride levels. In the aorta of HFD-fed mice, RS reduced vascular smooth muscle cell proliferation, macrophage accumulation, and elevation of VCAM-1 and inhibited the reduction of Robo4. Increased mRNA levels of Vcam1, Mmp9, and Srebp1 in atherosclerotic areas of HFD-fed mice were also suppressed with RS. Moreover, RS directly inhibited the migration of RAW264.7 cells in vitro. Thus, in HFD-fed ApoE-deficient mice, oral administration of RS ameliorated abnormal lipid metabolism and reduced vascular endothelial inflammation and hyperpermeability, macrophage infiltration and accumulation, and smooth muscle cell proliferation in the arteries leading to atherosclerosis. These results suggest that RS is an effective functional food for the prevention of atherosclerosis. Full article

(This article belongs to the Special Issue Research Advances Related to Cardiovascular System)

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12 pages, 2390 KiB

Open AccessArticle

Proteomic Analysis in Valvular Cardiomyopathy: Aortic Regurgitation vs. Aortic Stenosis

by Theresa Holst, Johannes Petersen, Sabine Ameling, Lisa Müller, Torsten Christ, Naomi Gedeon, Thomas Eschenhagen, Hermann Reichenspurner, Elke Hammer and Evaldas Girdauskas

Cells 2023, 12(6), 878; https://doi.org/10.3390/cells12060878 - 11 Mar 2023

Cited by 1 | Viewed by 1648

Abstract

Left ventricular (LV) reverse remodeling after aortic valve (AV) surgery is less predictable in chronic aortic regurgitation (AR) than in aortic stenosis (AS). We aimed to disclose specific LV myocardial protein signatures possibly contributing to differential disease progression. Global protein profiling of LV myocardial samples excised from the subaortic interventricular septum in patients with isolated AR or AS undergoing AV surgery was performed using liquid chromatography–electrospray ionization–tandem mass spectrometry. Based on label-free quantitation protein intensities, a logistic regression model was calculated and adjusted for age, sex and protein concentration. Web-based functional enrichment analyses of phenotype-associated proteins were performed utilizing g:Profiler and STRING. Data are available via ProteomeXchange with identifier PXD039662. Lysates from 38 patients, including 25 AR and 13 AS samples, were analyzed. AR patients presented with significantly larger LV diameters and volumes (end-diastolic diameter: 61 (12) vs. 48 (13) mm, p < 0.001; end-diastolic volume: 180.0 (74.6) vs. 92.3 (78.4), p = 0.001). A total of 171 proteins were associated with patient phenotype: 117 were positively associated with AR and the enrichment of intracellular compartment proteins (i.e., assigned to carbohydrate and nucleotide metabolism, protein biosynthesis and the proteasome) was detected. Additionally, 54 were positively associated with AS and the enrichment of extracellular compartment proteins (i.e., assigned to the immune and hematopoietic system) was observed. In summary, functional enrichment analysis revealed specific AR- and AS-associated signatures of LV myocardial proteins. Full article

(This article belongs to the Special Issue Research Advances Related to Cardiovascular System)

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12 pages, 3463 KiB

Open AccessArticle

Spectrin-Based Regulation of Cardiac Fibroblast Cell-Cell Communication

by Drew M. Nassal, Rebecca Shaheen, Nehal J. Patel, Jane Yu, Nick Leahy, Dimitra Bibidakis, Narasimham L. Parinandi and Thomas J. Hund

Cells 2023, 12(5), 748; https://doi.org/10.3390/cells12050748 - 26 Feb 2023

Cited by 1 | Viewed by 1714

Abstract

Cardiac fibroblasts (CFs) maintain the fibrous extracellular matrix (ECM) that supports proper cardiac function. Cardiac injury induces a transition in the activity of CFs to promote cardiac fibrosis. CFs play a critical role in sensing local injury signals and coordinating the organ level response through paracrine communication to distal cells. However, the mechanisms by which CFs engage cell-cell communication networks in response to stress remain unknown. We tested a role for the action-associated cytoskeletal protein β_IV-spectrin in regulating CF paracrine signaling. Conditioned culture media (CCM) was collected from WT and β_IV-spectrin deficient (qv^4J) CFs. WT CFs treated with qv^4J CCM showed increased proliferation and collagen gel compaction compared to control. Consistent with the functional measurements, qv^4J CCM contained higher levels of pro-inflammatory and pro-fibrotic cytokines and increased concentration of small extracellular vesicles (30–150 nm diameter, exosomes). Treatment of WT CFs with exosomes isolated from qv^4J CCM induced a similar phenotypic change as that observed with complete CCM. Treatment of qv^4J CFs with an inhibitor of the β_IV-spectrin-associated transcription factor, STAT3, decreased the levels of both cytokines and exosomes in conditioned media. This study expands the role of the β_IV-spectrin/STAT3 complex in stress-induced regulation of CF paracrine signaling. Full article

(This article belongs to the Special Issue Research Advances Related to Cardiovascular System)

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Review

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18 pages, 2233 KiB

Open AccessReview

Functions of RNA-Binding Proteins in Cardiovascular Disease

by Grégoire Ruffenach, Lejla Medzikovic, Wasila Sun, Jason Hong and Mansoureh Eghbali

Cells 2023, 12(24), 2794; https://doi.org/10.3390/cells12242794 - 08 Dec 2023

Cited by 1 | Viewed by 1130

Abstract

Gene expression is under tight regulation from the chromatin structure that regulates gene accessibility by the transcription machinery to protein degradation. At the transcript level, this regulation falls on RNA-binding proteins (RBPs). RBPs are a large and diverse class of proteins involved in all aspects of a transcript’s lifecycle: splicing and maturation, localization, stability, and translation. In the past few years, our understanding of the role of RBPs in cardiovascular diseases has expanded. Here, we discuss the general structure and function of RBPs and the latest discoveries of their role in pulmonary and systemic cardiovascular diseases. Full article

(This article belongs to the Special Issue Research Advances Related to Cardiovascular System)

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13 pages, 598 KiB

Open AccessReview

Lipoprotein(a)—60 Years Later—What Do We Know?

by Anna Pasławska and Przemysław J. Tomasik

Cells 2023, 12(20), 2472; https://doi.org/10.3390/cells12202472 - 17 Oct 2023

Cited by 3 | Viewed by 2497

Abstract

Lipoprotein(a) (Lp(a)) molecule includes two protein components: apolipoprotein(a) and apoB100. The molecule is the main transporter of oxidized phospholipids (OxPL) in plasma. The concentration of this strongly atherogenic lipoprotein is predominantly regulated by the LPA gene expression. Lp(a) is regarded as a risk factor for several cardiovascular diseases. Numerous epidemiological, clinical and in vitro studies showed a strong association between increased Lp(a) and atherosclerotic cardiovascular disease (ASCVD), calcific aortic valve disease/aortic stenosis (CAVD/AS), stroke, heart failure or peripheral arterial disease (PAD). Although there are acknowledged contributions of Lp(a) to the mentioned diseases, clinicians struggle with many inconveniences such as a lack of well-established treatment lowering Lp(a), and common guidelines for diagnosing or assessing cardiovascular risk among both adult and pediatric patients. Lp(a) levels are different with regard to a particular race or ethnicity and might fluctuate during childhood. Furthermore, the lack of standardization of assays is an additional impediment. The review presents the recent knowledge on Lp(a) based on clinical and scientific research, but also highlights relevant aspects of future study directions that would approach more suitable and effective managing risk associated with increased Lp(a), as well as control the Lp(a) levels. Full article

(This article belongs to the Special Issue Research Advances Related to Cardiovascular System)

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27 pages, 3351 KiB

Open AccessReview

K_V Channel-Interacting Proteins in the Neurological and Cardiovascular Systems: An Updated Review

by Le-Yi Wu, Yu-Juan Song, Cheng-Lin Zhang and Jie Liu

Cells 2023, 12(14), 1894; https://doi.org/10.3390/cells12141894 - 20 Jul 2023

Cited by 2 | Viewed by 1439

Abstract

K_V channel-interacting proteins (KChIP1-4) belong to a family of Ca²⁺-binding EF-hand proteins that are able to bind to the N-terminus of the K_V4 channel α-subunits. KChIPs are predominantly expressed in the brain and heart, where they contribute to the maintenance of the excitability of neurons and cardiomyocytes by modulating the fast inactivating-K_V4 currents. As the auxiliary subunit, KChIPs are critically involved in regulating the surface protein expression and gating properties of K_V4 channels. Mechanistically, KChIP1, KChIP2, and KChIP3 promote the translocation of K_V4 channels to the cell membrane, accelerate voltage-dependent activation, and slow the recovery rate of inactivation, which increases K_V4 currents. By contrast, KChIP4 suppresses K_V4 trafficking and eliminates the fast inactivation of K_V4 currents. In the heart, I_Ks, I_Ca,L, and I_Na can also be regulated by KChIPs. I_Ca,L and I_Na are positively regulated by KChIP2, whereas I_Ks is negatively regulated by KChIP2. Interestingly, KChIP3 is also known as downstream regulatory element antagonist modulator (DREAM) because it can bind directly to the downstream regulatory element (DRE) on the promoters of target genes that are implicated in the regulation of pain, memory, endocrine, immune, and inflammatory reactions. In addition, all the KChIPs can act as transcription factors to repress the expression of genes involved in circadian regulation. Altered expression of KChIPs has been implicated in the pathogenesis of several neurological and cardiovascular diseases. For example, KChIP2 is decreased in failing hearts, while loss of KChIP2 leads to increased susceptibility to arrhythmias. KChIP3 is increased in Alzheimer’s disease and amyotrophic lateral sclerosis, but decreased in epilepsy and Huntington’s disease. In the present review, we summarize the progress of recent studies regarding the structural properties, physiological functions, and pathological roles of KChIPs in both health and disease. We also summarize the small-molecule compounds that regulate the function of KChIPs. This review will provide an overview and update of the regulatory mechanism of the KChIP family and the progress of targeted drug research as a reference for researchers in related fields. Full article

(This article belongs to the Special Issue Research Advances Related to Cardiovascular System)

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32 pages, 8716 KiB

Open AccessReview

Human Health during Space Travel: State-of-the-Art Review

by Chayakrit Krittanawong, Nitin Kumar Singh, Richard A. Scheuring, Emmanuel Urquieta, Eric M. Bershad, Timothy R. Macaulay, Scott Kaplin, Carly Dunn, Stephen F. Kry, Thais Russomano, Marc Shepanek, Raymond P. Stowe, Andrew W. Kirkpatrick, Timothy J. Broderick, Jean D. Sibonga, Andrew G. Lee and Brian E. Crucian

Cells 2023, 12(1), 40; https://doi.org/10.3390/cells12010040 - 22 Dec 2022

Cited by 17 | Viewed by 11152

Abstract

The field of human space travel is in the midst of a dramatic revolution. Upcoming missions are looking to push the boundaries of space travel, with plans to travel for longer distances and durations than ever before. Both the National Aeronautics and Space Administration (NASA) and several commercial space companies (e.g., Blue Origin, SpaceX, Virgin Galactic) have already started the process of preparing for long-distance, long-duration space exploration and currently plan to explore inner solar planets (e.g., Mars) by the 2030s. With the emergence of space tourism, space travel has materialized as a potential new, exciting frontier of business, hospitality, medicine, and technology in the coming years. However, current evidence regarding human health in space is very limited, particularly pertaining to short-term and long-term space travel. This review synthesizes developments across the continuum of space health including prior studies and unpublished data from NASA related to each individual organ system, and medical screening prior to space travel. We categorized the extraterrestrial environment into exogenous (e.g., space radiation and microgravity) and endogenous processes (e.g., alteration of humans’ natural circadian rhythm and mental health due to confinement, isolation, immobilization, and lack of social interaction) and their various effects on human health. The aim of this review is to explore the potential health challenges associated with space travel and how they may be overcome in order to enable new paradigms for space health, as well as the use of emerging Artificial Intelligence based (AI) technology to propel future space health research. Full article

(This article belongs to the Special Issue Research Advances Related to Cardiovascular System)

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Other

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5 pages, 785 KiB

Open AccessComment

βIV-Spectrin in Cardiac Fibroblasts: Implications for Fibrosis and Therapeutic Targeting in Cardiac Diseases. Comment on Nassal et al. Spectrin-Based Regulation of Cardiac Fibroblast Cell-Cell Communication. Cells 2023, 12, 748

by Wenjing Xiang, Ning Zhou, Lei Li, Faming Chen, Lei Li and Ying Wang

Cells 2023, 12(17), 2186; https://doi.org/10.3390/cells12172186 - 31 Aug 2023

Viewed by 604

Abstract

Fibroblasts in the heart, traditionally recognized as interstitial cells, have long been overlooked in the study of cardiac physiology and pathology [...] Full article

(This article belongs to the Special Issue Research Advances Related to Cardiovascular System)

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