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Special Issue "The Molecular Mechanism of Cardiovascular Disease"

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A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Medical Research".

Deadline for manuscript submissions: closed (21 April 2023) | Viewed by 11602

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Special Issue Editors

Dr. Yufeng Yao

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Guest Editor

Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology and Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan 430074, China
Interests: cardiac hypertrophy; heart failure; vascular remolding

Dr. Zhen-Guo Ma

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Guest Editor

Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China
Interests: cardiac hypertrophy; heart failure; cardiac fibrosis

Dr. Lei Li
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Guest Editor

Department of Histology and Embryology, School of Basic Medical Sciences, Shandong University, Jinan 250012, China
Interests: cardio-vascular development and diseases

Special Issue Information

Dear Colleagues,

A Special Issue on the topic of “The Molecular Mechanism of Cardiovascular Disease” is being prepared for the journal Life (Impact Factor 3.817, ISSN 2075-1729).

Cardiovascular diseases (CVD) are diseases with the highest morbidity and mortality in the world. Today, despite many notable advances in molecular mechanisms, prognosis, diagnosis, and treatment, cardiovascular diseases remain the most frequent cause of mortality in all human populations. This Special Issue focuses on molecular mechanisms (vascular calcification, vascular remolding, endothelial dysfunction, inflammasome, oxidative stress, etc.) of CVD, contributing to better understanding their development and providing insights to more personalized medicine treatment.

We warmly welcome submissions, including original investigations, review articles, and communications on this topic.

Dr. Yufeng Yao
Dr. Zhen-Guo Ma
Dr. Lei Li
Guest Editors

Manuscript Submission Information

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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. Life is an international peer-reviewed open access monthly journal published by MDPI.

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Keywords

Heart failure
Cardiac hypertrophy
Vascular disease
Cardiovascular injury and repair

Published Papers (7 papers)

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Research

Open AccessArticle

Two Novel Functional Mutations in Promoter Region of SCN3B Gene Associated with Atrial Fibrillation

and

Life 2022, 12(11), 1794; https://doi.org/10.3390/life12111794 - 05 Nov 2022

Viewed by 697

Abstract

The sodium voltage-gated channel beta subunit 3 (SCN3B) plays a crucial role in electrically excitable cells and conduction tissue in the heart. Some previous studies have established that genetic modification in sodium voltage-channel genes encoding for the cardiac β-subunits, such as SCN1B, SCN2B, SCN3B and SCN4B, can result in atrial fibrillation (AF). In the current study, we identified two rare variants in 5′UTR (NM_018400.4: c.-324C>A, rs976125894 and NM_018400.4: c.-303C>T, rs1284768362) of SCN3B in two unrelated lone AF patients. Our further functional studies discovered that one of them, the A allele of c.-324C>A (rs976125894), can improve transcriptional activity and may raise SCN3B expression levels. The A allele of c.-324C>A (rs976125894) has higher transcriptional activity when it interacts with GATA4, as we confirmed transcription factor GATA4 is a regulator of SCN3B. To the best of our knowledge, the current study is the first to demonstrate that the gain-of-function mutation of SCN3B can produce AF and the first to link a mutation occurring in the non-coding 5′UTR region of SCN3B to lone AF. The work also offers empirical proof that GATA4 is a critical regulator of SCN3B gene regulation. Our findings may serve as an encyclopedia for AF susceptibility variants and can also provide insight into the investigation of the functional mechanisms behind AF variants discovered by genetic methods. Full article

(This article belongs to the Special Issue The Molecular Mechanism of Cardiovascular Disease)

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Open AccessArticle

Myostatin/AKT/FOXO Signaling Is Altered in Human Non-Ischemic Dilated Cardiomyopathy

Lea Hildebrandt

Maja-Theresa Dieterlen

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Life 2022, 12(9), 1418; https://doi.org/10.3390/life12091418 - 12 Sep 2022

Viewed by 927

Abstract

Disturbances in the ubiquitin proteasome system, and especially changes of the E3 ligases, are subjects of interest when searching for causes and therapies for cardiomyopathies. The aim of this study was to clarify whether the myostatin/AKT/forkhead box O (FOXO) pathway, which regulates the expression of the E3 ligases muscle atrophy F-box gene (MAFbx) and muscle ring-finger protein-1 (MuRF1), is changed in dilated cardiomyopathy of ischemic origin (IDCM) and dilated cardiomyopathy of non-ischemic origin (NIDCM). The mRNA and protein expression of myostatin, AKT, FOXO1, FOXO3, MAFbx and MuRF1 were quantified by real-time polymerase chain reaction and ELISA, respectively, in myocardial tissue from 26 IDCM and 23 NIDCM patients. Septal tissue from 17 patients undergoing Morrow resection served as a control. MAFbx and FOXO1 mRNA and protein expression (all p < 0.05), AKT mRNA (p < 0.01) and myostatin protein expression (p = 0.02) were decreased in NIDCM patients compared to the control group. Apart from decreases of AKT and MAFbx mRNA expression (both p < 0.01), no significant differences were detected in IDCM patients compared to the control group. Our results demonstrate that the myostatin/AKT/FOXO pathway is altered in NIDCM but not in IDCM patients. FOXO1 seems to be an important drug target for regulating the expression of MAFbx in NIDCM patients. Full article

(This article belongs to the Special Issue The Molecular Mechanism of Cardiovascular Disease)

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Open AccessEditor’s ChoiceArticle

Data Mining Identifies CCN2 and THBS1 as Biomarker Candidates for Cardiac Hypertrophy

Markus Johansson

Benyapa Tangruksa

Sepideh Heydarkhan-Hagvall

Anders Jeppsson

Peter Sartipy

and

Jane Synnergren

Life 2022, 12(5), 726; https://doi.org/10.3390/life12050726 - 12 May 2022

Cited by 1 | Viewed by 1774

Abstract

Cardiac hypertrophy is a condition that may contribute to the development of heart failure. In this study, we compare the gene-expression patterns of our in vitro stem-cell-based cardiac hypertrophy model with the gene expression of biopsies collected from hypertrophic human hearts. Twenty-five differentially expressed genes (DEGs) from both groups were identified and the expression of selected corresponding secreted proteins were validated using ELISA and Western blot. Several biomarkers, including CCN2, THBS1, NPPA, and NPPB, were identified, which showed significant overexpressions in the hypertrophic samples in both the cardiac biopsies and in the endothelin-1-treated cells, both at gene and protein levels. The protein-interaction network analysis revealed CCN2 as a central node among the 25 overlapping DEGs, suggesting that this gene might play an important role in the development of cardiac hypertrophy. GO-enrichment analysis of the 25 DEGs revealed many biological processes associated with cardiac function and the development of cardiac hypertrophy. In conclusion, we identified important similarities between ET-1-stimulated human-stem-cell-derived cardiomyocytes and human hypertrophic cardiac tissue. Novel putative cardiac hypertrophy biomarkers were identified and validated on the protein level, lending support for further investigations to assess their potential for future clinical applications. Full article

(This article belongs to the Special Issue The Molecular Mechanism of Cardiovascular Disease)

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Open AccessArticle

Role of Uncoupling Protein 2 Gene Polymorphisms on the Risk of Ischemic Stroke in a Sardinian Population

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Life 2022, 12(5), 721; https://doi.org/10.3390/life12050721 - 12 May 2022

Cited by 1 | Viewed by 1211

Abstract

The mitochondrial uncoupling protein 2 (UCP2) acts as an anion transporter and as an antioxidant factor able to reduce the reactive oxygen species level. Based on its effects, UCP2 prevents the membrane lipids, proteins, and DNA damage while preserving normal cellular functions. Many variants have been identified within the human UCP2. Some of them were associated with a higher risk of obesity, diabetes and cardiovascular diseases in different populations. UCP2 appears a suitable candidate also for the risk of ischemic stroke. In the current study, we investigated the possible association between few variants of UCP2 (rs659366, rs660339, rs1554995310) and the risk of ischemic stroke in a genetically homogenous cohort of cases and controls selected in Sardinia Island. This population has been previously analysed for other candidate genes. A total of 250 cases of ischemic stroke and 241 controls were enrolled in the study. The allelic/genotypic distribution of the 3 UCP2 variants was characterized and compared among cases and controls. The results of our study confirmed known risk factors for ischemic stroke: age, history of smoking, hypertension, hypercholesterolemia, and atrial fibrillation. No association was found between the 3 UCP2 variants and the risk of ischemic stroke in our Sardinian cohort. Full article

(This article belongs to the Special Issue The Molecular Mechanism of Cardiovascular Disease)

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Open AccessArticle

Characteristics of the Cardiosplenic Axis in Patients with Fatal Myocardial Infarction

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Life 2022, 12(5), 673; https://doi.org/10.3390/life12050673 - 01 May 2022

Viewed by 1414

Abstract

Myocardial ischemia triggers neurohumoral activation of the cardiosplenic axis. In rodents, adverse outcomes occur upon prolonged entrance of mononuclear cells from the spleen into myocardial tissue. The purpose of this study is to assess the features of spleen structure in patients with fatal myocardial infarction (MI), the dynamics of macrophage infiltration of the spleen and its relationship with cardiac macrophage infiltration and unfavorable outcomes. Using immunohistochemistry techniques, we analyzed the macrophage infiltration of the spleen and myocardium sections collected from patients (n = 30) with fatal MI. The spleen of the patients was decreased and showed a predominance of red pulp with a high concentration of CD68+ and stabilin-1+ cells. The white pulp contained many medium and small follicles and a lower concentration of CD68+ and stabilin-1+ cells, which was comparable to that in the infarct area of the myocardium. The concentration of CD68+ and stabilin-1+ cells increased in the myocardium in the late period of MI, but did not show any dynamics in the spleen. A high number of CD68+ cells in the red pulp and reduced concentration of stabilin-1+ cells in the white pulp were associated with unfavorable post-infarction outcomes. These fundamental findings could be a basis for the development of new personalized therapeutic and diagnostic approaches for the treatment of MI and its complications. Full article

(This article belongs to the Special Issue The Molecular Mechanism of Cardiovascular Disease)

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Open AccessArticle

Endothelial-Derived APT1-Mediated Macrophage-Endothelial Cell Interactions Participate in the Development of Atherosclerosis by Regulating the Ras/MAPK Signaling Pathway

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Life 2022, 12(4), 551; https://doi.org/10.3390/life12040551 - 07 Apr 2022

Cited by 2 | Viewed by 1312

Abstract

Acyl-protein thioesterase 1 (APT1) can affect H-Ras localization and function by promoting its depalmitoylation. However, relatively little attention has been paid to the effects of APT1 on H-Ras in the cardiovascular system. In this study, we revealed its roles in atherosclerosis development using oxidative low-density lipoprotein (ox-LDL)-induced endothelial dysfunction models and a Western diet-induced ApoE^−/− mouse model. The results showed that APT1 expression was up-regulated, while that of miR-138-5p (miR-138) was down-regulated (p < 0.05) in this model. In the meantime, APT1 and H-Ras were translocated from the cytoplasm to the plasma membrane. Bioinformatic analysis and double fluorescence identified miR-138 as the upstream regulator of APT1. APT1 knockdown regulated H-Ras localization and expression, which subsequently affected the MAPK signaling pathway and the expression of its downstream factors. Further research indicated that human umbilical vein endothelial cells (HUVECs)-derived biogenic nanoparticles (BiNPs), hBPs secretion, and RNA expression of hBP-loaded APT1 were increased (p < 0.05) in the ox-LDL induced endothelial dysfunction model. Meanwhile, the HUVECs-derived APT1 could further affect macrophage function through hBP transportation. Altogether, this study demonstrated that the miR-138-APT1 axis may be partially responsible for atherosclerosis development by regulating the H-Ras-MAPK signaling pathway and hBP transportation. The results also shed novel insight on the underlying mechanisms of, and identify potential diagnostic and therapeutic targets for, atherosclerotic cardiovascular diseases in the future. Full article

(This article belongs to the Special Issue The Molecular Mechanism of Cardiovascular Disease)

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Open AccessArticle

Multi-Omics Characterization of a Human Stem Cell-Based Model of Cardiac Hypertrophy

Markus Johansson

Benjamin Ulfenborg

Christian X. Andersson

Sepideh Heydarkhan-Hagvall

Anders Jeppsson

Peter Sartipy

and

Jane Synnergren

Life 2022, 12(2), 293; https://doi.org/10.3390/life12020293 - 16 Feb 2022

Cited by 3 | Viewed by 2663

Abstract

Cardiac hypertrophy is an important and independent risk factor for the development of cardiac myopathy that may lead to heart failure. The mechanisms underlying the development of cardiac hypertrophy are yet not well understood. To increase the knowledge about mechanisms and regulatory pathways involved in the progression of cardiac hypertrophy, we have developed a human induced pluripotent stem cell (hiPSC)-based in vitro model of cardiac hypertrophy and performed extensive characterization using a multi-omics approach. In a series of experiments, hiPSC-derived cardiomyocytes were stimulated with Endothelin-1 for 8, 24, 48, and 72 h, and their transcriptome and secreted proteome were analyzed. The transcriptomic data show many enriched canonical pathways related to cardiac hypertrophy already at the earliest time point, e.g., cardiac hypertrophy signaling. An integrated transcriptome–secretome analysis enabled the identification of multimodal biomarkers that may prove highly relevant for monitoring early cardiac hypertrophy progression. Taken together, the results from this study demonstrate that our in vitro model displays a hypertrophic response on both transcriptomic- and secreted-proteomic levels. The results also shed novel insights into the underlying mechanisms of cardiac hypertrophy, and novel putative early cardiac hypertrophy biomarkers have been identified that warrant further investigation to assess their potential clinical relevance. Full article

(This article belongs to the Special Issue The Molecular Mechanism of Cardiovascular Disease)

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