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Cardiovascular Diseases: From Pathology to Therapeutics
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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: 20 November 2025 | Viewed by 4869

Special Issue Editor

Dr. Woongbi Jang

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

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

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Published Papers (3 papers)

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Research

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15 pages, 263 KiB  
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
Viewed by 455
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

22 pages, 1950 KiB  
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 1226
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)
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23 pages, 4640 KiB  
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
Viewed by 2420
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)
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