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Advances in Cardiovascular and Vascular Biology

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

Deadline for manuscript submissions: closed (30 June 2026) | Viewed by 2054

Editor


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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,

Cardiovascular and vascular diseases remain the leading causes of morbidity and mortality worldwide, representing a major global health burden. These disorders encompass a wide range of pathological conditions, including atherosclerosis, ischemic heart disease, arrhythmias, heart failure, and microvascular dysfunction. Despite significant clinical advances, many aspects of their molecular and cellular pathogenesis remain incompletely understood, limiting the development of effective preventive and therapeutic strategies.

Recent progress in cardiovascular and vascular biology driven by advances in molecular biology, genomics, bioinformatics, imaging technologies, and systems medicine has substantially improved our understanding of disease mechanisms. Key processes such as oxidative stress, inflammation, endothelial dysfunction, metabolic remodeling, epigenetic regulation, and intercellular communication have emerged as central contributors to disease initiation and progression. These discoveries have also opened new avenues for biomarker discovery, risk stratification, and precision therapeutics.

This Special Issue aims to provide a comprehensive platform for cutting-edge research spanning fundamental biological mechanisms and translational innovations in cardiovascular and vascular diseases. In line with the scope of the International Journal of Molecular Sciences, the Issue will emphasize mechanistic insights and molecularly driven approaches with clear relevance to diagnosis, prognosis, and therapy. By bringing together original research articles and high-quality reviews, this collection seeks to foster cross-disciplinary dialogue and accelerate the translation of biological discoveries into clinical applications.

Topics of interest include, but are not limited to, the following:

  1. Molecular and cellular mechanisms underlying cardiovascular and vascular diseases;
  2. Endothelial biology, vascular remodeling, and microcirculatory dysfunction;
  3. Oxidative stress, inflammation, and metabolic regulation in cardiovascular pathology;
  4. Epigenetic regulation, non-coding RNAs, and gene regulatory networks;
  5. Biomarkers and molecular diagnostics for cardiovascular risk assessment;
  6. Translational and precision medicine approaches in cardiovascular diseases;
  7. Emerging therapeutic strategies, including pharmacologic, digital, and bioengineering-based interventions.

Dr. Woongbi Jang
Guest Editor

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Keywords

  • cardiovascular diseases
  • vascular biology
  • molecular mechanisms
  • biomarkers
  • endothelial dysfunction
  • translational medicine

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Published Papers (2 papers)

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Research

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18 pages, 4612 KB  
Article
ML216 Alleviates Age-Related Cardiac Fibrosis by Suppressing TGF-β1 Signaling Pathway
by Wenbin Liu, Feng Cui, Xiaodan Huang, Na Liang and Jun Li
Int. J. Mol. Sci. 2026, 27(8), 3425; https://doi.org/10.3390/ijms27083425 - 10 Apr 2026
Viewed by 1695
Abstract
Cardiac fibrosis is a hallmark of cardiac aging and a major contributor to development of heart failure. However, therapeutic strategies that specifically target cardiac fibrosis remain limited. In this study, we demonstrate that small-molecule compound ML216 exerts protective effects against aging-associated or β-adrenoceptor [...] Read more.
Cardiac fibrosis is a hallmark of cardiac aging and a major contributor to development of heart failure. However, therapeutic strategies that specifically target cardiac fibrosis remain limited. In this study, we demonstrate that small-molecule compound ML216 exerts protective effects against aging-associated or β-adrenoceptor agonist isoproterenol-induced cardiac fibrosis in vitro or in vivo. Mechanistically, ML216 inhibits transforming growth factor-β1 (TGF-β1) signaling by reducing TGF-β1 protein levels, thereby attenuating Mothers against decapentaplegic homolog (SMAD) phosphorylation and downstream induction of connective tissue growth factor (CTGF). This leads to a marked suppression of fibrotic genes Col1a1, Cnn2, and Acta2, ultimately resulting in reduced fibrosis. Additionally, the inhibition of the TGF-β1 pathway alleviates cardiomyocytes apoptosis, which may further limit inflammatory responses and contributes to the overall attenuation of cardiac fibrosis. Collectively, these findings demonstrate that ML216 mitigates cardiac fibrosis through the inhibition of TGF-β1 pathway-mediated fibrotic signaling and apoptosis, highlighting its potential as a therapeutic candidate for the treatment of cardiac fibrosis. Full article
(This article belongs to the Special Issue Advances in Cardiovascular and Vascular Biology)
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Review

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43 pages, 2776 KB  
Review
Pulsatility as a Potential Regulator of Cardiovascular Biology: Molecular, Cellular, and Hemodynamic Remodeling During Continuous-Flow Left Ventricular Assist Device Support and Following Heart Transplantation
by Przemysław Lutomski, Calogera Pisano, Krzysztof J. Filipiak, Giuseppe Maria Raffa, Roberta Vazzana, Ewelina Grywalska, Mansur Rahnama, Mariusz Kowalewski, Małgorzata Tomaszewska, Piotr Suwalski, Zbigniew Krasiński, Marek Jemielity, Jacek Zieliński and Tomasz Urbanowicz
Int. J. Mol. Sci. 2026, 27(15), 6650; https://doi.org/10.3390/ijms27156650 (registering DOI) - 25 Jul 2026
Abstract
Pulsatile blood flow is a fundamental characteristic of cardiovascular physiology that regulates endothelial function, vascular homeostasis, microcirculatory integrity, and organ adaptation through complex mechanobiological pathways. The widespread use of continuous-flow left ventricular assist devices (CF-LVADs) has created a unique clinical model of chronic [...] Read more.
Pulsatile blood flow is a fundamental characteristic of cardiovascular physiology that regulates endothelial function, vascular homeostasis, microcirculatory integrity, and organ adaptation through complex mechanobiological pathways. The widespread use of continuous-flow left ventricular assist devices (CF-LVADs) has created a unique clinical model of chronic pulsatility deprivation, whereas heart transplantation restores physiological pulsatile hemodynamics. This review examines the molecular, cellular, and systemic consequences of these contrasting circulatory states. Evidence from experimental and clinical studies indicates that reduced pulsatility during CF-LVAD support is associated with impaired endothelial mechanotransduction, glycocalyx disruption, oxidative stress, inflammatory activation, angiogenic dysregulation, acquired von Willebrand syndrome, and microvascular remodeling. These alterations contribute to bleeding, thrombosis, neurological events, and progressive end-organ dysfunction. In contrast, restoration of pulsatile flow following heart transplantation promotes recovery of endothelial signaling, nitric oxide bioavailability, vascular responsiveness, and tissue perfusion, although persistent immune-mediated injury may limit complete vascular normalization. Emerging concepts involving Piezo1 signaling, YAP/TAZ mechanotransduction, extracellular vesicles, immunometabolism, and multi-omics profiling further support the role of pulsatility as a biological regulator rather than a simple hemodynamic consequence of cardiac contraction. Understanding pulsatility-dependent cardiovascular remodeling may facilitate the development of next-generation circulatory support technologies and novel therapeutic strategies to preserve vascular health. Full article
(This article belongs to the Special Issue Advances in Cardiovascular and Vascular Biology)
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