Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.0
4.9
Journals
IJMS
Special Issues
Cardiovascular Diseases: From Pathology to Therapeutics
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Cardiovascular Diseases: From Pathology to Therapeutics

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 November 2025) | Viewed by 15870

Special Issue Editor

Dr. Woongbi Jang

E-Mail Website
Guest Editor
Department of Physiology, School of Medicine, Laboratory of Vascular Medicine & Stem Cell Biology, Pusan National University, Yangsan 626-870, Republic of Korea
Interests: cardioprotection; cardiotoxicity; cardiovascular disease; cardiac progenitor cells
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue will focus on cardiovascular diseases. Cardiovascular diseases (CVDs) encompass a wide range of conditions affecting the heart and blood vessels, representing a major global health challenge. This Special Issue is dedicated to exploring the comprehensive landscape of CVDs, from their underlying pathologies to therapeutic approaches that hold promise for improving patient outcomes.

In recent years, significant strides have been made in understanding the molecular and genetic basis of CVDs. This Special Issue seeks contributions that delve into the genetic factors contributing to CVD susceptibility, disease mechanisms, and novel therapeutic strategies. We welcome interdisciplinary research from fields such as cardiology, genetics, pharmacology, and regenerative medicine.

Researchers are invited to submit studies that shed light on the molecular pathways involved in CVD development and progression, as well as innovative therapies, including pharmacological interventions and regenerative therapies. By bridging the gap between pathologies and therapy, this Special Issue aims to advance our knowledge of CVDs and promote novel approaches to their prevention and treatment.

Dr. Woongbi Jang
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 250 words) can be sent to the Editorial Office for assessment.

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 diseases
  • pathologies
  • cardiac progenitor cells
  • molecular pathways
  • regenerative medicine

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.

Published Papers (5 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

15 pages, 263 KB  
Article
Biomarkers of Calcification, Endothelial Injury, and Platelet-Endothelial Interaction in Patients with Aortic Valve Stenosis
by Paweł Bańka, Klaudia Męcka, Adrianna Berger-Kucza, Karolina Wrona-Kolasa, Anna Rybicka-Musialik, Beata Nowak, Marek Elżbieciak, Magdalena Mizia-Szubryt, Wojciech Wróbel, Tomasz Francuz, Michał Lelek, Agnieszka Kosowska, Wojciech Garczorz, Tomasz Bochenek, Andrzej Swinarew, Jarosław Paluch, Maciej Wybraniec and Katarzyna Mizia-Stec
Int. J. Mol. Sci. 2025, 26(10), 4873; https://doi.org/10.3390/ijms26104873 - 19 May 2025
Cited by 2 | Viewed by 1387
Abstract
Aortic stenosis (AS) is a progressive valvular heart disease characterized by fibrocalcific remodeling, inflammation, and hemodynamic disturbances. Serum biomarkers may indirectly reflect these processes. Autotaxin (ATX) and lysophosphatidic acid (LPA) have been implicated in osteogenic differentiation of valvular interstitial cells, while growth differentiation [...] Read more.
Aortic stenosis (AS) is a progressive valvular heart disease characterized by fibrocalcific remodeling, inflammation, and hemodynamic disturbances. Serum biomarkers may indirectly reflect these processes. Autotaxin (ATX) and lysophosphatidic acid (LPA) have been implicated in osteogenic differentiation of valvular interstitial cells, while growth differentiation factor-15 (GDF-15) reflects cellular stress and vascular changes. Thrombomodulin (TM) indicates endothelial injury and interacts with thrombin. This study aimed to evaluate biomarkers focusing on serum ATX, LPA, GDF-15, and TM levels and flow-mediated dilatation (FMD) in patients with AS. Overall, 149 patients were included in the study: 86 consecutive patients with AS hospitalized due to qualification for invasive treatment of AS and 63 controls. The clinical characteristics, echocardiographic data, FMD, and the following biomarkers—ATX, LPA, GDF-15, and TM—were included in the analysis. AS patients presented increased serum levels of ATX, GDF-15, and TM as compared to the controls. Differences in LPA levels were not statistically significant. FMD values were significantly lower in AS patients. The biomarkers mentioned above and FMD correlated with AS severity. There were no differences in both biomarkers’ serum levels and FMD regarding the hemodynamic AS phenotype. GDF-15 serum level was a risk factor for all-cause mortality and MACCE in the 12-month follow-up. Full article
(This article belongs to the Special Issue Cardiovascular Diseases: From Pathology to Therapeutics)

Review

Jump to: Research

41 pages, 2067 KB  
Review
Emerging Technologies for Exploring the Cellular Mechanisms in Vascular Diseases
by Debasis Sahu, Treena Ganguly, Avantika Mann, Yash Gupta, Logan R. Van Nynatten and Douglas D. Fraser
Int. J. Mol. Sci. 2026, 27(1), 164; https://doi.org/10.3390/ijms27010164 - 23 Dec 2025
Viewed by 819
Abstract
Vascular diseases (VDs) and cardiovascular diseases (CVDs) are the leading causes of morbidity and mortality worldwide. Current diagnostic and therapeutic approaches are limited by insufficient resolution and a lack of mechanistic understanding at the cellular level. Traditional imaging and clinical assays do not [...] Read more.
Vascular diseases (VDs) and cardiovascular diseases (CVDs) are the leading causes of morbidity and mortality worldwide. Current diagnostic and therapeutic approaches are limited by insufficient resolution and a lack of mechanistic understanding at the cellular level. Traditional imaging and clinical assays do not fully capture the dynamic molecular and structural complexities underlying vascular pathology. Recent technological innovations, including single-cell and spatial transcriptomics, super-resolution and photoacoustic imaging, microfluidic organ-on-chip platforms, Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)/CRISPR-associated protein 9 (Cas9)-based gene editing, and artificial intelligence (AI), have created new opportunities for investigating the cellular and molecular basis of VDs. These techniques enable high-resolution mapping of cellular heterogeneity and functional alterations, facilitating the integration of large-scale data for biomarker discovery, disease modeling, and therapeutic development. This review focuses on evaluating the translational readiness, limitations, and potential clinical applications of these emerging technologies. Understanding the cellular and molecular mechanisms of VDs is essential for developing targeted therapies and precise diagnostics. Integrating single-cell and multiomics approaches highlights disease-driving cell types and gene programs. Optogenetics and organ-on-chip platforms allow for controlled manipulation and physiologically relevant modeling, while AI enhances data integration, risk prediction, and clinical interpretability. Future efforts should prioritize multi-center, large-scale validation studies, harmonization of assay protocols, and integration with clinical datasets and human samples. Multi-omics approaches and computational modeling hold promise for unraveling disease complexity, while advances in regulatory science and digital simulation (such as digital twins) may further accelerate personalized medicine in vascular disease research and treatment. Full article
(This article belongs to the Special Issue Cardiovascular Diseases: From Pathology to Therapeutics)
►▼ Show Figures

Graphical abstract

26 pages, 2343 KB  
Review
Molecular Mechanisms of Microvascular Obstruction and Dysfunction in Percutaneous Coronary Interventions: From Pathophysiology to Therapeutics—A Comprehensive Review
by Andre M. Nicolau, Pedro G. Silva, Hernan Patricio G. Mejía, Juan F. Granada, Grzegorz L. Kaluza, Daniel Burkhoff, Thiago Abizaid, Brunna Pileggi, Antônio F. D. Freire, Roger R. Godinho, Carlos M. Campos, Fabio S. de Brito, Jr., Alexandre Abizaid and Pedro H. C. Melo
Int. J. Mol. Sci. 2025, 26(14), 6835; https://doi.org/10.3390/ijms26146835 - 16 Jul 2025
Cited by 6 | Viewed by 4325
Abstract
Coronary microvascular obstruction and dysfunction (CMVO) frequently arise following primary percutaneous coronary intervention (PCI), particularly in individuals with myocardial infarction. Despite the restoration of epicardial blood flow, microvascular perfusion might still be compromised, resulting in negative clinical outcomes. CMVO is a complex condition [...] Read more.
Coronary microvascular obstruction and dysfunction (CMVO) frequently arise following primary percutaneous coronary intervention (PCI), particularly in individuals with myocardial infarction. Despite the restoration of epicardial blood flow, microvascular perfusion might still be compromised, resulting in negative clinical outcomes. CMVO is a complex condition resulting from a combination of ischemia, distal thrombotic embolization, reperfusion injury, and individual susceptibilities such as inflammation and endothelial dysfunction. The pathophysiological features of this condition include microvascular spasm, endothelial swelling, capillary plugging by leukocytes and platelets, and oxidative stress. Traditional angiographic assessments, such as Thrombolysis in Myocardial Infarction (TIMI) flow grade and myocardial blush grade, have limited sensitivity. Cardiac magnetic resonance imaging (CMR) stands as the gold standard for identifying CMVO, while the index of microvascular resistance (IMR) is a promising invasive option. Treatment approaches involve powerful antiplatelet drugs, anticoagulants, and supersaturated oxygen, yet no treatment has been definitively shown to reverse established CMVO. CMVO remains a significant therapeutic challenge in coronary artery disease management. Enhancing the comprehension of its core mechanisms is vital for the development of more effective and personalized treatment strategies. Full article
(This article belongs to the Special Issue Cardiovascular Diseases: From Pathology to Therapeutics)
►▼ Show Figures

Figure 1

22 pages, 1950 KB  
Review
Targeting Mitochondrial Dysfunction to Prevent Endothelial Dysfunction and Atherosclerosis in Diabetes: Focus on the Novel Uncoupler BAM15
by Woong Bi Jang, Vinoth Kumar Rethineswaran and Sang-Mo Kwon
Int. J. Mol. Sci. 2025, 26(10), 4603; https://doi.org/10.3390/ijms26104603 - 11 May 2025
Viewed by 4624
Abstract
Diabetes mellitus is a chronic metabolic disorder characterized by persistent hyperglycemia, leading to endothelial dysfunction and accelerated atherosclerosis. Mitochondrial dysfunction, oxidative stress, and dysregulated lipid metabolism contribute to endothelial cell (EC) injury, promoting plaque formation and increasing cardiovascular disease risk. Current lipid-lowering therapies [...] Read more.
Diabetes mellitus is a chronic metabolic disorder characterized by persistent hyperglycemia, leading to endothelial dysfunction and accelerated atherosclerosis. Mitochondrial dysfunction, oxidative stress, and dysregulated lipid metabolism contribute to endothelial cell (EC) injury, promoting plaque formation and increasing cardiovascular disease risk. Current lipid-lowering therapies have limited effectiveness in restoring endothelial function, highlighting the need for novel strategies. Mitochondrial uncoupling has emerged as a promising approach, with BAM15—a newly identified mitochondrial uncoupler—showing potential therapeutic benefits. BAM15 enhances fatty acid oxidation (FAO), reduces reactive oxygen species, and protects ECs from hyperglycemia-induced apoptosis. Unlike conventional uncouplers, BAM15 demonstrates improved tolerability and efficacy without severe off-target effects. It restores mitochondrial function, improves endothelial survival, and supports metabolic homeostasis under hyperglycemic conditions. This review uniquely integrates emerging evidence on mitochondrial dysfunction, endothelial metabolism, and FAO to highlight the novel role of BAM15 in restoring vascular function in diabetes. We provide the first focused synthesis of BAM15’s mechanistic impact on EC bioenergetics and position it within the broader landscape of mitochondrial-targeted therapies for diabetic vascular complications. Further research is needed to elucidate the molecular mechanism through which BAM15 modulates EC metabolism and to evaluate its long-term vascular effects in diabetic models. Full article
(This article belongs to the Special Issue Cardiovascular Diseases: From Pathology to Therapeutics)
►▼ Show Figures

Figure 1

23 pages, 4640 KB  
Review
Mouse Models of HIV-Associated Atherosclerosis
by Victoria R. Stephens, Sharareh Ameli, Amy S. Major and Celestine N. Wanjalla
Int. J. Mol. Sci. 2025, 26(7), 3417; https://doi.org/10.3390/ijms26073417 - 5 Apr 2025
Cited by 1 | Viewed by 3649
Abstract
Cardiovascular disease (CVD) remains the leading cause of death worldwide. Several factors are implicated in the pathogenesis of CVD, and efforts have been made to reduce traditional risks, yet CVD remains a complex burden. Notably, people living with HIV (PLWH) are twice as [...] Read more.
Cardiovascular disease (CVD) remains the leading cause of death worldwide. Several factors are implicated in the pathogenesis of CVD, and efforts have been made to reduce traditional risks, yet CVD remains a complex burden. Notably, people living with HIV (PLWH) are twice as likely to develop CVD compared to persons without HIV (PWoH). Intensive statin therapy, the first-line treatment to prevent cardiovascular events, is effective at reducing morbidity and mortality. However, statin therapy has not reduced the overall prevalence of CVD. Despite antiretroviral therapy (ART), and new guidelines for statin use, PLWH have persistent elevation of inflammatory markers, which is suggested to be a bigger driver of future cardiovascular events than low-density lipoprotein. Herein, we have summarized the development of atherosclerosis and highlighted mouse models of atherosclerosis in the presence and absence of HIV. Since most mouse strains have several mechanisms that are atheroprotective, researchers have developed mouse models to study CVD using dietary and genetic manipulations. In evaluating the current methodologies for studying HIV-associated atherosclerosis, we have detailed the benefits of integrating multi-omics analyses, genetic manipulations, and immune cell profiling within mouse models. These advanced approaches significantly enhance our capacity to address critical gaps in understanding the immune mechanisms driving CVD, including in the context of HIV. Full article
(This article belongs to the Special Issue Cardiovascular Diseases: From Pathology to Therapeutics)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-5
Back to TopTop