Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.1
4.9
Journals
IJMS
Special Issues
Editorial Board Members’ Collection Series: Cardiovascular Diseases
ijms-logo
Submit to Special Issue Submit Abstract to Special Issue Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Editorial Board Members’ Collection Series: Cardiovascular Diseases

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: 20 June 2025 | Viewed by 4275

Special Issue Editors

Dr. Melania Gaggini

E-Mail Website
Guest Editor
Istituto di Fisiologia Clinica, National Research Council of Italy, Via Moruzzi 1, I-56124 Pisa, Italy
Interests: metabolic disease; organ pathophysiology; cardiovascular disease; metabolomic ad lipidomic technology
Special Issues, Collections and Topics in MDPI journals
Dr. Cristina Vassalle

E-Mail Website
Guest Editor
Fondazione CNR-Regione Toscana G. Monasterio, Via Moruzzi 1, I-56124 Pisa, Italy
Interests: cardiometabolic risk; cardiometabolic disease; biomarkers; endothelial function; sphingolipids
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality globally, taking an estimated 17.9 million lives each year. Additionally, cardiometabolic syndrome represents a constellation of metabolic abnormalities including diabetes, insulin resistance, hypertension, and fatty liver disease, which are in turn key risk factors for cardiovascular disease. Several circulating biomarkers and metabolites, such as lipids and amino acids, are regulators of biological processes associated with normal cell function and metabolism. In particular, changes in lipid components and amino acid profiles can have a significant role in cell function, antioxidant defenses, the immune system, and inflammatory responses. We invite investigators to contribute either original research or review articles to this special issue, focusing on the role and mechanisms of significant circulating biomarkers and cellular pathways that drive or participate in the onset and development of obesity, diabetes, non-alcoholic fatty liver disease, atherosclerosis, hypertension, and coronary artery diseases. Subtopics may include, but are not limited to, the following issues:

  • Insulin resistance, glucose fatty acid metabolism, and cardiometabolic disease;
  • Assessment of biochemical and molecular biomarkers related to cardiometabolic risk and prevention;
  • Amino acid profiles and their relationship with coronary artery disease;
  • Lipid species and other key biomarkers and pathways implicated in the development of cardiometabolic disease.

Dr. Melania Gaggini
Dr. Cristina Vassalle
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

  • cardiovascular disease
  • metabolism
  • cardiometabolic risk
  • coronary artery disease
  • CVD

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Related Special Issues

Published Papers (3 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

21 pages, 8007 KiB  
Article
Role of LMCD1 in the Long-Term Effects of Angiotensin II in Vascular Smooth Muscle Cells
by Janka Borbála Gém, Kinga Bernadett Kovács, Szilvia Barsi, Saba Hadadnejadtehrani, Amir Damouni, Gábor Turu, András Dávid Tóth, Péter Várnai, László Hunyady and András Balla
Int. J. Mol. Sci. 2025, 26(9), 4053; https://doi.org/10.3390/ijms26094053 - 25 Apr 2025
Viewed by 248
Abstract
Excessive activity of the hormone angiotensin II (AngII) is known to contribute to the pathogenesis of multiple cardiovascular diseases, including atherosclerosis, vascular remodeling, and hypertension, primarily through inducing gene expression changes. In this study, we identified LMCD1 (LIM and cysteine-rich domains 1, also [...] Read more.
Excessive activity of the hormone angiotensin II (AngII) is known to contribute to the pathogenesis of multiple cardiovascular diseases, including atherosclerosis, vascular remodeling, and hypertension, primarily through inducing gene expression changes. In this study, we identified LMCD1 (LIM and cysteine-rich domains 1, also known as Dyxin), primarily recognized as a transcription co-factor involved in various oncogenic processes, cardiac hypertrophy, and vascular remodeling, as a potential key factor in AngII-mediated effects in vascular smooth muscle cells (VSMCs). We demonstrated that AngII upregulates LMCD1 expression in primary rat VSMCs through type 1 angiotensin receptor (AT1-R) activation, leading to calcium signaling and p38 MAPK pathway activation. Additionally, we also demonstrated in A7r5 vascular smooth muscle cells that LMCD1 protein overexpression results in enhanced cell proliferation and cell migration. Our findings provide insights into the mechanisms by which AngII mediates changes in LMCD1 expression. The elevated expression of LMCD1 enhanced the cell proliferation and migration in VSMCs in vitro experiments, suggesting that LMCD1 may be an important factor in vascular remodeling and the pathogenesis of severe cardiovascular diseases. These results raise the possibility that LMCD1 could be a promising pharmacological target in the cardiovascular dysfunctions associated with AT1-R overactivation. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Cardiovascular Diseases)
►▼ Show Figures

Figure 1

18 pages, 5972 KiB  
Article
Extracellular PKM2 Preserves Cardiomyocytes and Reduces Cardiac Fibrosis During Myocardial Infarction
by Yang Huang, Bin Li, Zongxiang Gui, Erhe Gao, Yi Yuan, Jenny Yang, Khan Hekmatyar, Falguni Mishra, Payton Chan and Zhiren Liu
Int. J. Mol. Sci. 2024, 25(24), 13246; https://doi.org/10.3390/ijms252413246 - 10 Dec 2024
Viewed by 1203
Abstract
Substantial loss of cardiomyocytes during heart attacks and onset of other cardiovascular diseases is a major cause of mortality. Preservation of cardiomyocytes during cardiac injury would be the most effective strategy to manage these diseases in clinic. However, there is no effective treatment [...] Read more.
Substantial loss of cardiomyocytes during heart attacks and onset of other cardiovascular diseases is a major cause of mortality. Preservation of cardiomyocytes during cardiac injury would be the most effective strategy to manage these diseases in clinic. However, there is no effective treatment strategy that is able to prevent cardiomyocyte loss. We demonstrate here that the systemic administration of a recombinant PKM2 mutant (G415R) preserves cardiomyocytes and reduces cardiac fibrosis during myocardial infarction. G415R preserves cardiomyocytes by protecting the cardiomyocytes from dying and by promoting cardiomyocyte proliferation. Preservation of cardiomyocytes by extracellular PKM2 (EcPKM2) reduces cardiac fibrosis because of the decreased activation of cardiac fibroblasts. Our experiments show that EcPKM2 (G415R) exerts its action by interacting with integrin avb3 on cardiomyocytes. EcPKM2(G415R) activates the integrin–FAK–PI3K signaling axis, which subsequently suppresses PTEN expression and consequently regulates cardiomyocyte apoptosis resistance and proliferation under hypoxia and oxidative stress conditions. Our studies uncover an important cardiomyocyte protection mechanism. More importantly, the activity/action of EcPKM2 (G415R) in preserving cardiomyocyte suggesting a possible therapeutic strategy and target for the treatment of heart attacks and other cardiovascular diseases. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Cardiovascular Diseases)
►▼ Show Figures

Figure 1

Review

Jump to: Research

23 pages, 2272 KiB  
Review
Effect of Oxidative Stress on Mitochondrial Damage and Repair in Heart Disease and Ischemic Events
by Paweł Kowalczyk, Sebastian Krych, Karol Kramkowski, Agata Jęczmyk and Tomasz Hrapkowicz
Int. J. Mol. Sci. 2024, 25(22), 12467; https://doi.org/10.3390/ijms252212467 - 20 Nov 2024
Cited by 2 | Viewed by 2300
Abstract
The literature analysis conducted in this review discusses the latest achievements in the identification of cardiovascular damage induced by oxidative stress with secondary platelet mitochondrial dysfunction. Damage to the platelets of mitochondria as a result of their interactions with reactive oxygen species (ROS) [...] Read more.
The literature analysis conducted in this review discusses the latest achievements in the identification of cardiovascular damage induced by oxidative stress with secondary platelet mitochondrial dysfunction. Damage to the platelets of mitochondria as a result of their interactions with reactive oxygen species (ROS) and reactive nitrogen species (RNS) can lead to their numerous ischemic events associated with hypoxia or hyperoxia processes in the cell. Disturbances in redox reactions in the platelet mitochondrial membrane lead to the direct oxidation of cellular macromolecules, including nucleic acids (DNA base oxidation), membrane lipids (lipid peroxidation process) and cellular proteins (formation of reducing groups in repair proteins and amino acid peroxides). Oxidative changes in biomolecules inducing tissue damage leads to inflammation, initiating pathogenic processes associated with faster cell aging or their apoptosis. The consequence of damage to platelet mitochondria and their excessive activation is the induction of cardiovascular and neurodegenerative diseases (Parkinson’s and Alzheimer’s), as well as carbohydrate metabolism disorders (diabetes). The oxidation of mitochondrial DNA can lead to modifications in its bases, inducing the formation of exocyclic adducts of the ethano and propano type. As a consequence, it disrupts DNA repair processes and conduces to premature neoplastic transformation in critical genes such as the p53 suppressor gene, which leads to the development of various types of tumors. The topic of new innovative methods and techniques for the analysis of oxidative stress in platelet mitochondria based on methods such as a nicking assay, oxygen consumption assay, Total Thrombus formation Analysis System (T-Tas), and continuous-flow left ventricular assist devices (CF-LVADs) was also discussed. They were put together into one scientific and research platform. This will enable the facilitation of faster diagnostics and the identification of platelet mitochondrial damage by clinicians and scientists in order to implement adequate therapeutic procedures and minimize the risk of the induction of cardiovascular diseases, including ischemic events correlated with them. A quantitative analysis of the processes of thrombus formation in cardiovascular diseases will provide an opportunity to select specific anticoagulant and thrombolytic drugs under conditions of preserved hemostasis. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: Cardiovascular Diseases)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop