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Novel Insights in Molecular Mechanisms of Cardiovascular Diseases
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Novel Insights in Molecular Mechanisms of Cardiovascular Diseases

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

Deadline for manuscript submissions: closed (20 July 2023) | Viewed by 3677

Special Issue Editors

Dr. Xiao-heng Liu

E-Mail Website
Guest Editor
Institute of Biomedical Engineering, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu 610041, China
Interests: cardiovascular and cerebrovascular diseases; malignant tumors; signal transduction mechanisms; drug targets
Dr. Yi Tan

E-Mail Website
Guest Editor
School of Medicine, University of Louisville, Louisville, KY 40292, USA
Interests: the role of SDF-1/CXCR4/CXCR7 axes in diabetic complications; the role of FGFs (e.g.: FGF1, FGF5, FGF16, FGF21, etc.) in diabetic complications; antioxidative mechanisms of metallothionein and Nrf2 in diabetic complications

Special Issue Information

Dear Colleagues, 

Cardiovascular diseases (CVDs) are the leading cause of death worldwide and a major barrier to sustainable human development. Cardiovascular diseases are a group of disorders of the heart and blood vessels which include coronary heart disease, cerebrovascular disease, peripheral arterial disease, rheumatic heart disease, congenital heart disease, deep vein thrombosis, and pulmonary embolism. In recent years, many risk factors, such as unhealthy diet, physical inactivity, tobacco use, and harmful use of alcohol, have been found to contribute to the initiation and progress of cardiovascular disease. However, the detailed molecular mechanisms of cardiovascular disease were far from clear. Therefore, understanding the cellular and molecular mechanisms of cardiovascular diseases is imperative, which could help us to develop effective and timely strategies to cope with the challenges of cardiovascular disease epidemics.

This special issue aims to collect original and review articles to enhance insight into cardiovascular disease mechanisms and the perspective for innovation. Suggested topics include, but are not limited to:

  • Cellular mechanisms (vascular calcification, vascular remolding, endothelial dysfunction, phenotypic switching, inflammation, cell death, etc.) of cardiovascular disease and the signaling pathways involved in,
  • Effects of extracellular vesicles on the development of cardiovascular disease and the related diagnostic and therapeutic methods,
  • New drug development,
  • Novel indications for older drugs,
  • Genetic approach to treatment,
  • New directions in device and cell therapy

This special issue is assisted by our Topical Advisory Panel Member Dr. Hongchi Yu from Sichuan University.

Dr. Xiao-heng Liu
Dr. Yi Tan
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. 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

  • atherosclerosis
  • vascular calcification
  • extracellular vesicles
  • diagnosis
  • therapy

Published Papers (3 papers)

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Research

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14 pages, 3145 KiB  
Article
Cardiomyocyte-Restricted Expression of IL11 Causes Cardiac Fibrosis, Inflammation, and Dysfunction
by Mark Sweeney, Katie O’Fee, Chelsie Villanueva-Hayes, Ekhlas Rahman, Michael Lee, Konstantinos Vanezis, Ivan Andrew, Wei-Wen Lim, Anissa Widjaja, Paul J. R. Barton and Stuart A. Cook
Int. J. Mol. Sci. 2023, 24(16), 12989; https://doi.org/10.3390/ijms241612989 - 20 Aug 2023
Cited by 3 | Viewed by 1409
Abstract
Cardiac fibrosis is a common pathological process in heart disease, representing a therapeutic target. Transforming growth factor β (TGFβ) is the canonical driver of cardiac fibrosis and was recently shown to be dependent on interleukin 11 (IL11) for its profibrotic effects in fibroblasts. [...] Read more.
Cardiac fibrosis is a common pathological process in heart disease, representing a therapeutic target. Transforming growth factor β (TGFβ) is the canonical driver of cardiac fibrosis and was recently shown to be dependent on interleukin 11 (IL11) for its profibrotic effects in fibroblasts. In the opposite direction, recombinant human IL11 has been reported as anti-fibrotic and anti-inflammatory in the mouse heart. In this study, we determined the effects of IL11 expression in cardiomyocytes on cardiac pathobiology and function. We used the Cre-loxP system to generate a tamoxifen-inducible mouse with cardiomyocyte-restricted murine Il11 expression. Using protein assays, bulk RNA-sequencing, and in vivo imaging, we analyzed the effects of IL11 on myocardial fibrosis, inflammation, and cardiac function, challenging previous reports suggesting the cardioprotective potential of IL11. TGFβ stimulation of cardiomyocytes caused Il11 upregulation. Compared to wild-type controls, Il11-expressing hearts demonstrated severe cardiac fibrosis and inflammation that was associated with the upregulation of cytokines, chemokines, complement factors, and increased inflammatory cells. IL11 expression also activated a program of endothelial-to-mesenchymal transition and resulted in left ventricular dysfunction. Our data define species-matched IL11 as strongly profibrotic and proinflammatory when secreted from cardiomyocytes and further establish IL11 as a disease factor. Full article
(This article belongs to the Special Issue Novel Insights in Molecular Mechanisms of Cardiovascular Diseases)
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14 pages, 2617 KiB  
Article
ETV2 Enhances CXCL5 Secretion from Endothelial Cells, Leading to the Promotion of Vascular Smooth Muscle Cell Migration
by Ningning Sun, Beyongsam Chu, Dong-Hyun Choi, Leejin Lim and Heesang Song
Int. J. Mol. Sci. 2023, 24(12), 9904; https://doi.org/10.3390/ijms24129904 - 08 Jun 2023
Cited by 1 | Viewed by 1069
Abstract
Abnormal communication between endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) promotes vascular diseases, including atherogenesis. ETS variant transcription factor 2 (ETV2) plays a substantial role in pathological angiogenesis and the reprogramming of ECs; however, the role of ETV2 in the communication [...] Read more.
Abnormal communication between endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) promotes vascular diseases, including atherogenesis. ETS variant transcription factor 2 (ETV2) plays a substantial role in pathological angiogenesis and the reprogramming of ECs; however, the role of ETV2 in the communication between ECs and VSMCs has not been revealed. To investigate the interactive role of ETV2 in the EC to VSMC phenotype, we first showed that treatment with a conditioned medium from ETV2-overexpressed ECs (Ad-ETV2 CM) significantly increased VSMC migration. The cytokine array showed altered levels of several cytokines in Ad-ETV2 CM compared with those in normal CM. We found that C-X-C motif chemokine 5 (CXCL5) promoted VSMC migration using the Boyden chamber and wound healing assays. In addition, an inhibitor of C-X-C motif chemokine receptor 2 (CXCR2) (the receptor for CXCL5) significantly inhibited this process. Gelatin zymography showed that the activities of matrix metalloproteinase (MMP)-2 and MMP-9 increased in the media of VSMCs treated with Ad-ETV2 CM. Western blotting revealed a positive correlation between Akt/p38/c-Jun phosphorylation and CXCL5 concentration. The inhibition of Akt and p38-c-Jun effectively blocked CXCL5-induced VSMC migration. In conclusion, CXCL5 from ECs induced by ETV2 promotes VSMC migration via MMP upregulation and the activation of Akt and p38/c-Jun. Full article
(This article belongs to the Special Issue Novel Insights in Molecular Mechanisms of Cardiovascular Diseases)
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Review

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17 pages, 692 KiB  
Review
Potential Roles of microRNAs for Assessing Cardiovascular Risk in Pre-Eclampsia-Exposed Postpartum Women and Offspring
by Nurul Iffah Mohd Isa, Saiful Effendi Syafruddin, Mohd Helmy Mokhtar, Shahidee Zainal Abidin, Farah Hanan Fathihah Jaffar, Azizah Ugusman and Adila A. Hamid
Int. J. Mol. Sci. 2023, 24(23), 16842; https://doi.org/10.3390/ijms242316842 - 28 Nov 2023
Viewed by 810
Abstract
Pre-eclampsia, which is part of the spectrum of hypertensive pregnancy disorders, poses a significant health burden, contributing to maternal and infant morbidity and mortality. Pre-eclampsia is widely associated with persistent adverse effects on the cardiovascular health of women with a history of pre-eclampsia. [...] Read more.
Pre-eclampsia, which is part of the spectrum of hypertensive pregnancy disorders, poses a significant health burden, contributing to maternal and infant morbidity and mortality. Pre-eclampsia is widely associated with persistent adverse effects on the cardiovascular health of women with a history of pre-eclampsia. Additionally, there is increasing evidence demonstrating that offspring of pre-eclamptic pregnancies have altered cardiac structure and function, as well as different vascular physiology due to the decrease in endothelial function. Therefore, early detection of the likelihood of developing pre-eclampsia-associated cardiovascular diseases is vital, as this could facilitate the undertaking of the necessary clinical measures to avoid disease progression. The utilisation of microRNAs as biomarkers is currently on the rise as microRNAs have been found to play important roles in regulating various physiological and pathophysiological processes. In regard to pre-eclampsia, recent studies have shown that the expression of microRNAs is altered in postpartum women and their offspring who have been exposed to pre-eclampsia, and that these alterations may persist for several years. This review, therefore, addresses changes in microRNA expression found in postpartum women and offspring exposed to pre-eclampsia, their involvement in cardiovascular disease, and the potential role of microRNAs to be used as predictive tools and therapeutic targets in future cardiovascular disease research. Full article
(This article belongs to the Special Issue Novel Insights in Molecular Mechanisms of Cardiovascular Diseases)
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